Methods of use for plasmalogen precursors in treating plasmalogen-associated diseases

Abstract

This disclosure relates to methods of using certain precursor compounds such as lysoalkylphosphatidylcholines, (LPC(O)s) to increase the levels of plasmalogens in the subject to provide improved health outcomes. More specifically, this disclosure relates to the use of the precursor compounds to treat liver diseases and controlling weight.

Description

METHODS OF USE FOR PLASMALOGEN PRECURSORS IN TREATINGPLASMALOGEN-ASSOCIATED DISEASESTECHNICAL FIELD

[0001] This disclosure relates to methods of using certain precursor compounds such as lysoalkylphosphatidylcholines, (LPC(O)s) to increase the levels of plasmalogens in the subject to provide improved health outcomes. More specifically, this disclosure relates to the use of the precursor compounds to treat liver diseases and controlling weight.BACKGROUND

[0002] Plasmalogens, as defined herein, comprise a group of plasmenyl-phospholipids which are a major cell membrane component. As part of the broader class of phospholipids, plasmanyl- and / or plasmenyl-phospholipids are a unique class of ether phospholipids that are major components of cell membranes. Their biophysical role in cell membranes has been studied while knowledge concerning their biological roles is an important area of new research. Plasmalogens are primarily present as alkenylphosphatidylcholine (PC) and alkenylphosphatidylethanolamine (PE) species, a.k.a. PC(P) and PE(P), respectively. They are characterized by a cv.s- vinyl ether bond linking an alkyl chain to the sn-1 carbon position of the glycerol backbone. They also optionally have an acyl linked fatty acid ester bond in the sn-2 carbon position. Plasmalogens are often esterified with polyunsaturated fatty acids such as arachidonic acid (20:4, ARA) and the omega-3 fatty acid docosahexaenoic acid (22:6 (DHA), a major constituent of fish oil), whereas the vinyl ether linked residue is usually otherwise saturated (i.e., no double bonds are present in the chain other than the vinyl ether group) or otherwise monounsaturated (i.e., one double bond is present in the chain in addition to the vinyl ether group).

[0003] Plasmalogen biosynthesis is a complex process involving multiple enzymes within the peroxisome and endoplasmic reticulum. The rate-limiting step in this pathway is the formation of the long chain fatty alcohol by fatty acyl-CoA reductase 1 and 2 (Far- 1 / 2). It is possible to bypass the rate-limiting step in plasmalogen synthesis through the oral administration of naturally occurring alkylglycerols (1-O-alkylglycerol or l-O-alkyl-2,3-diacylglycerol). These can be incorporated directly into the phospholipid pathway, and so bypass the peroxisome. This leads to an increase in circulating and tissue plasmalogens. Although alkylglycerols are present in our diet, the levels in typical diets are insufficient to significantly boost human plasmalogen levels. Shark liver oil is rich in alkylglycerols and is currently used as a dietary supplement to reduceinflammation and improve immune function. Alkylglycerols can also be synthesized, providing a future avenue for an environmentally sustainable source of these compounds (Magnusson, C.D., et al., Tetrahedron (2011) 67: 1821-36; Shi, Y., et al., Green Chemistry (2010) 12(12)).

[0004] WO 2021 / 007623 Al to Baker Heart and Diabetes Institute, which is incorporated by reference herein in its entirety, relates generally to various compositions and methods for maintaining or modulating mixtures of ether lipid molecules in human tissues, used for non-disease conditions and for treating certain disease conditions including obesity, diabetes, fatty liver disease, cardiovascular disease, and Alzheimer’s disease. PCT / US2024 / 010129 and PCT / EP2024 / 053394, also to Baker Heart and Diabetes Institute, which are incorporated by reference herein in their entireties, relate to improved compositions for maintaining or modulating mixtures of ether lipid molecules in human tissues and their use for improving non-disease conditions and for treating certain disease conditions.

[0005] More than 2 billion people worldwide are overweight or obese in spite of public health policies and individual treatment efforts (Gonzalez-Muniesa, P., et al., (2017) Nature Reviews Disease Primers 3). Individuals with obesity have a body mass index greater than 30, often consuming many more calories than burned by exercise and typical daily activity. Obesity is a chronic and complex disease characterized by excessive fat deposits that can impair health and cause disease. Obesity is associated with a higher risk of developing certain diseases and illnesses, including liver disease, cardiovascular disease, metabolic syndrome, and type 2 diabetes, hereby referred to as metabolic disorders or metabolic diseases. Controlling body weight by preventing weight gain or promoting weight loss is recommended to avoid the development of such comorbidities. Therefore, it remains a need in the art to provide efficacious, safe, and tolerable treatment for weight control to achieve long term health.

[0006] Type II Diabetes (T2D) is now considered a global pandemic, and considered the most common metabolic disorder, with projections of over 590 million cases by 2035. The cause is multifactorial in nature but the physical result is impaired insulin functioning (Reed, J., et al., Diabetes, Metabolic Syndrome and Obesity (2021) 14:3567-3602). T2D and obesity have a strong correlation with each other, and type II diabetes is one of the cluster of diseases that are often linked to metabolic syndrome, which is thought to be influenced by the following risk factors: high blood sugar, low HDL cholesterol, high triglycerides, high blood pressure, and large waist circumference. Recently, Glucagon-like Peptide I Receptor (GLP-1R) agonist drugs have showngreat promise in reducing a number of these risks for metabolic syndrome as well as treating T2D; however, the high cost of the medicines is prohibitive, and they are generally not approved by insurance companies for preventative treatment (Reed, J., et al., Diabetes, Metabolic Syndrome and Obesity (2021) 14:3567-3602) or weight loss. Additionally, these medicants are often not tolerated well by individuals and / or can be accompanied by significant muscle loss as well. Frequently, once the GLP-1 drug is stopped, the weight also rebounds. Therefore, there is significant interest in finding alternatives for GLP-1 or less expensive interventions to provide weight loss maintenance after GLP-1 treatment. Therefore, there remains a need for additional dietary supplements or medications for the clinical treatment of T2D.

[0007] The LDL from obese patients with metabolic syndrome and patients with type II diabetes have been found to have decreased ethanolamine plasmalogen levels (22% and 49% respectively), increased lipid peroxidation, decreased cholesterol ester, and increased triglyceride compared to controls (Braverman, N.E., and Moser, A.B., Biochimica et Biophysica Acta (2012)). It is thought that lipid signaling pathways may be a root cause, or at least a contributing part of, type II diabetes.

[0008] Diabetic retinopathy caused by retinal microaneurysms (MA) is one of the most common side effects of both type I and type II diabetes. In one study, the impact of plasmalogens and other lipids to modulate MA found that serum plasmalogen dml6:0 may reduce the risk of MA in diabetic patients (de Mello, V.D. et al. Nutrients (2021) 13:4452). Another study found a correlation with increased serum plasmalogens (induced by myo-inositol) and positive outcomes for metabolic syndrome patients with hyperlipidemia (Maeba R., et al., J Nutr Sci Vitaminol (2008)54:3). These clinical studies did not include LPX(O)s.

[0009] There exists an unmet need for improved methods of treating diabetes and other comorbidities associated with metabolic syndrome. To date no experiments have been done with administration of the ether lipid compounds LPC(O) and LPE(O) in metabolic syndrome or T2D models.

[0010] Non-alcoholic fatty liver disease (NAFLD) has also emerged as a significant global health burden, affecting a substantial portion of the population worldwide (Chalasani, N., et al., Hepatology (2018) 67: 1; Samy, A.M., et al., Heliyon (2024) 10:9, E30387). NAFLD encompasses a spectrum of conditions, ranging from simple steatosis (accumulation of triglycerides within hepatocytes) to non-alcoholic steatohepatitis (NASH), which involves hepatic inflammation, fibrosis, and potential progression to cirrhosis or hepatocellular carcinoma(Grander, C., et al., Cardiovasc Res (2023) 119:9). Despite the escalating prevalence and severity of NAFLD, effective therapeutic strategies remain limited.

[0011] The alarming rise in the incidence and complexity of NAFLD necessitates urgent research efforts to elucidate its underlying pathophysiological mechanisms and develop innovative therapeutic interventions (Parola, M., and Pinzani, M., Molecular Aspects of Medicine (2024) 95: 10121; Harrison, S.A., Allen, A.M., Dubourg, J., et al., Nat Med (2023) 29:562-573). While the aetiology of NAFLD is multifactorial, dysregulated lipid metabolism has been identified as a key driver in disease progression. Recent studies have shed light on the critical role of plasmalogens, a unique class of glycerophospholipids, in maintaining hepatic lipid homeostasis. Plasmalogens possess a vinyl-ether bond at the sn-1 position of the glycerol backbone, rendering them distinct from conventional glycerophospholipids. They play crucial roles in cellular membranes, particularly in protecting cells from oxidative stress due to their ability to scavenge reactive oxygen species. They are essential for the proper function of the nervous system, heart, and immune cells, contributing to membrane fluidity and signaling processes. Additionally, plasmalogens are involved in the synthesis of other critical lipids and support the structural integrity of cells (B raverman, N.E. and Moser, A.B., Biochim Biophys Acta (2012) 1822:9). Importantly, alterations in plasmalogen levels have been observed in NAFLD patients, suggesting a potential association with disease pathogenesis (Puri, P., et al., Hepatology (2009) 50:6; Tiwari-Heckler, S., et al., Nutrients (2018) 10:5). Dietary supplementation of sources of plasmalogens or their precursors eg alkyl glycerols, from marine sources, has been investigated as a means to enhance plasmalogen levels and potentially attenuate NAFLD progression (Jang, J.E., et al., Hepatology (2017) 66:2; Liu, Y., et al., Redox Biology (2021) 43; Wang, Z., et al., Journal of Agricultural and Food Chemistry, (2024). 72: 17; Ikuta, A., et al., Clinica Chimica Acta (2019) 493 : 1-7). These authors showed that alkylglycerols were able to prevent hepatic steatosis and NASH in mice and proposed a mechanism, suggesting that raising hepatic plasmalogen levels could be a viable treatment for NASH.

[0012] Heart diseases are the number one cause of death in most western countries. The economic impact and resource burden of cardiovascular disease and heart failure in the United States is large, estimated to be over 43 billion USD in 2020 and projected to hit over 69 billion USD by 2030 (Urbich, M., Globe, G., Pantiri, K. et al. A Systematic Review of Medical Costs Associated with Heart Failure in the USA (2014-2020); PharmacoEconomics (2020), 38, 1219-1236). Historically emphasis has been placed on prevention and detection of arterial plaques to prevent heart attacks through diet, exercise, and use of drugs in the statin family. Much focus was on lipid levels such as cholesterol. More recently other contributors have been studied involving mitochondrial dysfunction and oxidative stress (Bozelli, JC Jr et al, Plasmalogens and Chronic Inflammatory Diseases, REVIEW article Front. Physiol., (2021), Sec. Lipid and Fatty Acid Research). There exists an unmet need for an improved method of treating cardiovascular disease.

[0013] A link between plasmalogens and heart diseases has been postulated not only for genetic mutations such as Barth Syndrome, but also coronary artery disease (CAD). A number of publications have explored possible roles of plasmalogens in contributing to heart disease (Rasmiena AA, Barlow CK, Stefanovic N, Huynh K, Tan R, Sharma A, Tull D, de Haan JB, Meikle PJ. Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE / GPxl- deficient mice. Atherosclerosis. (2015) 243(2):598-608; Meikle, 2011; Paul, 2019).Plasmalogen levels are notably different in those with CAD (Bozelli, 2021).

[0014] Plasmalogen levels have also been associated with neurological disease and neurodevelopment including Alzheimer's disease (AD), peroxisomal disorders, brain development, neural recovery, and movement disorders such as Multiple Sclerosis (MS) and Parkinson’s Disease (PD).

[0015] Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain, which is characterized by mild cognitive impairment (MCI), memory deterioration, behavioral disturbances, impairment and loss of independent function. AD is caused by multiple factors and involving multiple genes, with the end result being dysfunction of dendrites and death of neurons. A recent review article (Hajjo et al, Review of the Recent Advances in Alzheimer’s Disease Research and the Utilization of Network Biology Approaches for Prioritizing Diagnostics and Therapeutics; Diagnostics 2022, 12, 2975.) estimates that over 6.5 million Americans have Alzheimer’s dementia with numbers expected to double by 2060 with the aging population.

[0016] AD is a complicated disease, characterized by an accumulation of insoluble aggregates of amyloid-beta peptide (A0) and abnormal tau proteins. (Igarashi, M. et al. Disturbed choline plasmalogen and phospholipid fatty acid concentrations in Alzheimer disease prefrontal cortex.” J Alzheimer’s Dis. (2011) 24(3): 507-517). Tau is found in multiple tissues,but is particularly abundant in axons of neurons while the A0 aggregates are associated with inflammatory responses. Together, tau and A0 form neurofibrillary inclusions, which are a hallmark of Alzheimer’s disease, and are believed to be responsible for associated cognitive impairment.

[0017] Plasmalogens have a vinyl ether bond at the sn-1 position and an ester bond at the sn-2 location and are a major component of cell membranes, being associated with normal synaptic structure and function as well as neurotransmitter release (Li, R. et al. Plasmalogen Improves Memory Function by Regulating Neurogenesis in a Mouse Model of Alzheimer’s Diseases, Int. J. Mol. Sci.,(2023) 24, 12234). More recently a link between plasmalogens and neurogenesis has been shown, with plasmalogens thought to have neuroprotective properties that positively impact hippocampus-dependent cognitive function (Li, R et al, 2023). Bozelli et al (Bozelli, J.C. Jr et al, Plasmalogens and Chronic Inflammatory Diseases, REVIEW article Front. Physiol., 20 October 2021, Sec. Lipid and Fatty Acid Research, Volume 12 - 2021) have illustrated the importance of plasmalogen levels in regard to a large number of diseases, and indicated that brain gray and white matter contain 10-12 percent of total phospholipids as plasmalogens, predominantly PE plasmalogens (PC plasmalogens were not detected). In AD patients approximately 40% decrease in plasmalogens is noted in white matter, and 10-30% decrease in plasmalogens in gray matter is also noted, depending on the severity of dementia. It is thought that decreased plasmalogen levels are due to decreased peroxisomes in neurites and increased oxidative stress. While a number of plasmalogen replacement therapy attempts have been described (Bozelli J.C. Jr, Epand RM. Plasmalogen Replacement Therapy. Membranes (Basel). 2021 Oct 29; 11(11): 838) for treatment of AD, to date no experiments have been done with consumption of the ether lipid compounds LPC(O) and LPE(O) in AD models.

[0018] Many previous treatments developed for Alzheimer’s disease have been proven to be ineffective at preventing neuronal degeneration and death associated with Alzheimer's disease or even treatments which are able to slow or that alleviate symptoms.

[0019] The only approved drugs on the market are for symptom management in early stages of the disease. The combination of the enormous healthcare cost burden and no cure available creates an increasing public health crisis. There exists an unmet need for an improved method of treating Alzheimer’s disease.

[0020] Parkinson’s disease (PD) is the second largest neurodegenerative disease next to Alzheimer’s Disease (AD), and like AD, to date there is no cure. Parkinson’s disease is broadly characterized as a movement or motor disorder. The cause of PD is thought to be related to environmental factors as well as being polygenic in nature (S. Paul, et al., Plasmalogens: A potential therapeutic target for neurodegenerative and cardiometabolic disease, Progress in Lipid Research, Volume 74, 2019, Pages 186-195.) Some symptoms can be treated in the case of PD by increasing dopamine levels that are deficient. However non-motor symptoms (e.g. dementia, depression, and sleep problems) are not improved and remain a target for drug discovery (S. Mawatari et al, Improvement of Blood Plasmalogens and Clinical Symptoms in Parkinson’s Disease by Oral Administration of Ether Phospholipids: A Preliminary Report, Hindawi Parkinson’s Disease, 2020, 2671070). PD is thought to affect 1-2% of people over the age of 60, and the aging population will soon increase the expected burden on the healthcare system.

[0021] Bozelli et al (Bozelli, JC Jr et al, Plasmalogens and Chronic Inflammatory Diseases, REVIEW article Front. Physiol., 20 October 2021, Sec. Lipid and Fatty Acid Research, Volume 12 - 2021) have illustrated the importance of plasmalogen levels in regards to a large number of diseases, and indicated that a 20-60% loss in plasmalogens is associated with Parkinson’s disease. Fabelo et al (Fabelo, N., et al. (2011). Severe alterations in lipid composition of frontal cortex lipid rafts from Parkinson’s disease and incidental Parkinson’s disease. Mol. Med. 17, 1107-1118) showed that frontal cortex lipid rafts had significant loss of plasmalogen. The mechanism is thought to be due to increased oxidative stress. Predominantly, the ethanolamine-containing plasmalogen levels are impacted.

[0022] While various plasmalogen replacement therapies have been attempted (Bozelli J.C. Jr, Epand RM. Plasmalogen Replacement Therapy. Membranes (Basel). 2021 Oct 29; 11(11): 838; Mawatari et al. (2020)), to date no experiments have been done with LPC(O) and LPE(O) in Parkinson’s models. Thus, there exists an unmet need for an improved method to treat treating a movement or motor disorder, such as Parkinson’s disease, and / or symptoms thereof.

[0023] Orphan diseases such as peroxisomal diseases, are associated with a deficiency of plasmalogen production.

[0024] Rhizomelic chondrodysplasia punctata (RCDP) is a peroxisomal disorder that is considered rare, impacting only less than 1 in 100,000 people. However, it causes severe skeletal abnormalities, respiratory problems, seizures, cataracts, and intellectual disabilities and mostimpacted children do not survive into adulthood (Steinberg SJ et al. Peroxisome biogenesis disorders. Biochim Biophys Acta. 2006 Dec; 1763(12): 1733-48.). RCDP is caused by mutations to one or more of the PEX7, GNPAT, and AGPS genes which are involved in the formation of plasmalogens in peroxisomes. Peroxisomes are needed for proper lipid metabolism of lipids associated with the central nervous system and digestion (Dominger F et al, Homeostasis of phospholipids — The level of phosphatidylethanolamine tightly adapts to changes in ethanolamine plasmalogens, Biochim Biophys Acta 2015 Feb, 1851(2): 117-128). Plasmalogens are found in cell membranes of various tissues throughout the human body and are essential for proper function (Bozelli, 2021; Terlecky 2006).

[0025] Zellweger’s Syndrome (ZS) is another peroxisomal disorder, where peroxisomes are absent, which impacts nearly every organ of the body (Steinberg SJ et al., 2006). Twelve different possible modifications of PEX genes can be found in ZS patients, with the predominant number of cases involving mutations to PEX1. Children bom with ZS generally do not survive past infancy.

[0026] Bozelli et al (Bozelli, JC Jr et al, Plasmalogens and Chronic Inflammatory Diseases, REVIEW article Front. Physiol., 20 October 2021, Sec. Lipid and Fatty Acid Research) have illustrated the importance of plasmalogen levels in regards to a large number of diseases, and indicated that in RCDP there is a variable decrease in plasmalogen levels that correlates to disease severity; primarily ethanolamine plasmalogens that appear to be impacted. In ZS there are very low levels of plasmalogens, they are nearly absent, and both choline and ethanolamine plasmalogens are impacted.

[0027] Fallatah et al (Fallatah W, et al. Oral administration of a synthetic vinyl-ether plasmalogen normalizes open field activity in a mouse model of rhizomelic chondrodysplasia punctata. Dis Model Meeh. (2020), 13) showed that oral administration of a synthetic plasmalogen PPI-1040 normalized some hyperactive behavior and some plasmalogen levels; but a plasmalogen precursor did not. Plasmalogen replacement therapy has been done in a number of model systems (Bozelli JC Jr, Epand RM. Plasmalogen Replacement Therapy. Membranes (Basel). (2021); 11, 838), but to date no experiments have been done with oral administration of the ether lipid compounds LPC(O) and LPE(O) in RCDP or ZS models, as the compounds are largely unavailable.

[0028] There exists an unmet need for an improved method of treating orphan diseases such as peroxisomal diseases.

[0029] Multiple Sclerosis (MS) is a complex neurodegenerative disease of the central nervous system and thought to be an autoimmune disorder (Huang, W.J., et al., Exp. Ther. Med. (2017) 13:3163-3166). The disease is thought to impact over 2 million people, and largely affects young adults (Bargiela D., and Chinnery P.F., Neuroscience Letters (2019) 710: 132932). MS results in plaques forming in the brain and spinal cord. Incorrect functioning of the mitochondria leads to neuroinflammation (Bozelli, JC Jr et al., Front. Physiol. (2021) 12). Inflammatory lesions impact numerous systems in the human body such as vision, muscle weakness, balance, loss of feeling, and bladder or bowel problems (Huang, W.J., et al., Exp. Ther. Med. (2017) 13:3163- 3166). No cure is available, though some treatments are used to alleviate symptoms, and several antibody-based drugs have shown promise in reducing relapses.

[0030] Studies have found a decrease in plasmalogen levels in a large number of diseases, including MS where there is a general decrease in plasmalogen levels, including both ethanolamine and choline forms (Bozelli, JC Jr et al., Front. Physiol. (2021) 12). The mechanism is thought to be due to increased oxidative stress and demyelination. Since myelin sheaths are rich in plasmalogen, other studies suggest that MS is a metabolic disease associated with dysregulation of lipids, and recent therapeutic interventions have been undertaken using lipids to modulate inflammation and neurodegeneration (Podbielska M., et al., Int J Mol Sci. (2021) 7:22).

[0031] There exists an unmet need for improved methods of treating multiple sclerosis.

[0032] The WHO recommends breastfeeding exclusively for 6 months and continuing with food supplementation up to 2 years and beyond (https: / / www.who.int / health-topics / breastfeeding). The benefits of breastfeeding are known to improve the health of infants, and not just through the passage of antibodies (https: / / www.breastfeeding.asn.au / resources / breastfeeding-and-immunity). The importance of human milk oligosaccharides (prebiotics) has emerged more recently and these products are being added to infant formulas (Wicinski, M et al., "Human Milk Oligo-saccharides: Health Benefits, Potential Applications in Infant Formulas, and Pharmacology" (2020), Nutrients 12, no. 1 : 266).

[0033] Similarly, the benefits of breastfeeding on cognition and health are well documented (Lee H, et al., "Effect of Breastfeeding Duration on Cognitive Development in Infants: 3-Year Follow-up Study" (31 Apr 2016), J Korean Med Sci. 31(4): 579-84; McGowan C and Bland R,"The Benefits of Breastfeeding on Child Intelligence, Behavior, and Executive Function: A Review of Recent Evidence" (18 Mar 2023), Breastfeed Med. (3): 172-187). Omega-6 and omega- 3 fatty acids ARA and DHA have been studied and are thought to be important for brain development, and these are supplemented in infant formulas at levels typically measured in human breast milk — 0.2-0.4% of total fatty acids as DHA and 0.35-0.7% as ARA. C. Kuratko et al., "Enrichment of infant formula with omega-3 fatty acids" (01 Jan 2013), In Food enrichment with omega-3 fatty acids (pp. 353-386), Woodhead Publishing.

[0034] A more comprehensive investigation of the lipid profile of human milk has been conducted recently and shows a further gap in infant formula composition and human breast milk (AD George et al, "Defining the lipid profiles of human milk, infant formula, and animal milk: implications for infant feeding" (2023 Aug 30), Front Nutr.; 10: 1227340). This suggests that other types of lipids or nutrients from mothers’ milk should be explored to improve the development of infant formulas, given that a large percentage of the world population cannot breast feed as recommended by the WHO.

[0035] Additionally, the impact of supplementing expectant and lactating mothers with additional nutrients is being explored. Recent results suggest that not all unsaturated fatty acids are beneficial (R K Vinding, et al, "Fish oil supplementation during pregnancy, anthropometries, and metabolic health at age ten: A randomized clinical trial" (2024), The American Journal of Clinical Nutrition, Volume 119, Issue 4, Pages 960-968). Here n-3 LCPUFA supplementation led to higher BMI and metabolic syndrome scores at age 6 and 10.

[0036] Testing of additional lipid types is warranted. Plasmalogens are known to have a wide array of benefits in adult health and cognition (West et al, "How Do Ethanolamine Plasmalogens Contribute to Order and Structure of Neurological Membranes?" J Phys Chem B. 2020 Feb 6;124(5):828-839; Goodenowe et al, "Targeted Plasmalogen Supplementation: Effects on Blood Plasmalogens, Oxidative Stress Biomarkers, Cognition, and Mobility in Cognitively Impaired Persons", Front. Cell Dev. Biol., 06 July 2022, Volume 10; Bozaelli et al., "Plasmalogens and Chronic Inflammatory Diseases", Front Physiol. 2021 Oct 21;12:730829) which has led to a number of studies of plasmalogen replacement therapy in mammalian models (Bozzeli and Epand, "Plasmalogen Replacement Therapy", Membranes (Basel). 2021 Oct 29; 11(11): 838).

[0037] There exists an unmet need for an improved method of increasing the levels of plasmalogens for infants, including dietary supplements for breast-feeding mothers and nutritional formulations for infants (including infant formulas).

[0038] Plasmalogens are not readily available and are not stable in the gastrointestinal tract. Additional experimentation is warranted to develop methods to modulate the levels of plasmalogens in circulation and in liver tissues.SUMMARY

[0039] The present inventors have surprisingly found that administration of the plasmalogen precursors, LPC(O) and LPE(O) provide meaningful benefit in the modulation of plasmalogen levels and in the treatment of plasmalogen-associated disorders, such as metabolic disorders and neurological disorders. To date no experiments have been done with administration of the ether lipid compounds LPC(O) and LPE(O) in multiple sclerosis. Plasmalogens are not readily available and are not stable in the gastrointestinal tract. Additional experimentation is warranted to develop methods to modulate the levels of plasmalogens in circulation to treat multiple sclerosis through feeding of more efficacious and stable plasmalogen precursors. The present disclosure provides novel methods for treating multiple sclerosis by modulating plasmalogen levels with LPX(O) compounds. Neurodevelopment of infants is another potential application of the LPX(O) plasmalogen precursor compounds, as well as other benefits for prenatal and breastfeeding mothers, and neonates. Plasmalogens and their precursors may provide benefits to infants as well, through supplementation to a pregnant or nursing mother and / or supplementation of infant formula. The present disclosure presents certain plasmalogen precursors that have the ability to survive the digestive tract and enter the blood plasma and other tissues not only to treat diseases, but also to improve the levels of plasmalogens in rapidly developing infants.

[0040] The present disclosure provides novel and inventive methods for treating liver disease and controlling weight by modulating plasmalogen levels with LPX(O) compounds.

[0041] It has been found that the ingestion of lysoalkylphosphatidylcholine, a.k.a. LPC(O), and alkylphosphatidylcholine, a.k.a. PC(O), in krill oil led to the elevation of PE(P) and PC(P) species. This is not obvious as it is generally considered that LPC(O) and PC(O) are a dead end on the plasmalogen biosynthetic pathway and that there is no active pathway for the conversion ofLPC(O) and PC(O) into PE(P) and PC(P). Thus, it appears that the LPC(O) / PC(O) are able to be shunted into the plasmalogen biosynthetic pathway and / or they are able to directly stimulate the natural biosynthetic pathway to increase plasmalogen synthesis.

[0042] Comparison of the increase in the level of plasmalogen in circulation (plasma) after a given treatment of LPC(O) and PC(O) (krill oil) with the elevation following a similar treatment of AKDAG (shark liver oil) identified that the LPC(O) and PC(O) were more bioavailable. That is, it was surprisingly discovered that a smaller dose of LPC(O) and PC(O) could lead to the same increase in circulating levels of plasmalogens as would be obtained by administering a comparatively larger dose of AKDAG (shark liver oil).

[0043] It is notable that phospholipids found in krill oil differ substantially from that in humans; however, there is an expectation that LPC(O) levels are connected to plasmalogens, or at the least, are involved with the modulation of plasmalogens in humans.

[0044] Additionally, it was recognized that the composition of the alkyl chains in LPC(O) and PC(O) in krill oil was substantially different from the composition of alkenyl chains in plasmalogens in humans and so could potentially influence the composition of the resulting plasmalogens as had been previously reported for alkylglycerol (AKG) and alkyldiacylglycerol (AKDAG) (WO 2021 / 007623). This led to the present development and disclosure of formulations and compositions for use in liver disease and controlling weight. The formulations and compositions disclosed herein may take the form of one or more of a medicament, a pharmaceutical, a dietary supplement, a medical food and a food product or other nutritional composition.BRIEF DESCRIPTION OF THE DRAWINGS

[0045] Further aspects of the present disclosure will be more readily appreciated upon review of the detailed description of its various embodiments, described below, when taken in conjunction with the accompanying drawings.

[0046] FIG. 1 describes changes in plasma ether lipid classes (% change) from baseline / pre-treatment following krill oil (KO), fish oil (FO) or shark liver oil (SLO) supplementation. Changes in plasma ether lipid classes were grouped by supplement. Subjects showed significant percent changes in ether lipid classes after KO (measured at 15 and 30 days) and SLO treatments (measured at 21 days). FO supplementation did not have a significant impacton plasma ether lipid classes. The nominal significance of the treatment effect was determined using paired t- tests (Krill oil baseline vs Krill oil 15 days, Krill oil baseline vs Krill oil 30 days, Fish oil baseline vs Fish oil 15 days, Fish oil baseline vs Fish oil 30 days; SLO pre-treatment vs SLO 21 days); * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001.

[0047] FIG. 2 describes changes in plasma ether lipid classes (% change) from baseline / pre-treatment following KO, FO or SLO supplementation (grouped by lipid class). The effects of different supplements were grouped by plasma ether lipid classes. Subjects showed significant percent changes in ether lipid classes after KO (measured at 15 and 30 days) and SLO treatments (measured at 21 days). FO supplementation did not have a significant impact on plasma ether lipid classes. The nominal significance of the treatment effect was determined using paired t- tests (Krill oil baseline vs Krill oil 15 days, Krill oil baseline vs Krill oil 30 days, Fish oil baseline vs Fish oil 15 days, Fish oil baseline vs Fish oil 30 days; SLO pre-treatment vs SLO 21 days); * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001.

[0048] FIG. 3 describes the effect of KO supplementation on alkenyl chain composition of PE plasmalogens. Data are presented as Mean±SD. KO supplementation did not have a significant impact on alkenyl chain composition of PE plasmalogen. The nominal significance of the treatment effect was determined using Repeated Measures ANOVA followed by Tukey’s multiple comparison tests; * indicated P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001.

[0049] FIG. 4 describes the effect of FO supplementation on alkenyl chain composition of PE plasmalogens. Data are presented as Mean±SD. FO supplementation did not have a significant impact on alkenyl chain composition of PE plasmalogen. The nominal significance of the treatment effect was determined using Repeated Measures ANOVA followed by Tukey’s multiple comparison tests; * indicated P < 0.05.

[0050] FIG. 5 describes the effect of SLO supplementation on alkenyl chain composition of PE plasmalogens. Data are presented as Mean±SD. SLO supplementation significantly altered the alkenyl chain composition of PE plasmalogen. There was an increase in the proportion of 18: 1 alkenyl chain containing PE plasmalogens and a decrease in the proportions of 16:0 and 18:0 alkenyl chain containing PE plasmalogens. The nominal significance of the treatment effect was determined using paired t- tests; ** indicates P < 0.01 and *** indicates P < 0.001.

[0051] FIG. 6 describes the effect of KO supplementation on acyl chain composition of PE plasmalogens. Data are presented as Mean±SD. KO supplementation decreased the proportionof 18: 1, 18:2 and 20:4 containing PE plasmalogens and increased the proportions of 20:5 and 22:6 containing PE plasmalogens. The nominal significance of the treatment effect was determined using Repeated Measures ANOVA followed by Tukey’s multiple comparison tests; ** indicates P < 0.01 and *** indicates P < 0.001.

[0052] FIG. 7 describes the effect of FO supplementation on acyl chain composition of PE plasmalogens. Data are presented as Mean±SD. FO supplementation decreased the proportion of 18: 1, 18:2 and 20:4 containing PE plasmalogens and increased the proportions of 20:5 and 22:6 containing PE plasmalogens. The nominal significance of the treatment effect was determined using Repeated Measures ANOVA followed by Tukey’s multiple comparison tests; * indicated P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001.

[0053] FIG. 8 describes the effect of SLO supplementation on acyl chain composition of PE plasmalogens. Data are presented as Mean±SD. SLO supplementation decreased 20:4 containing PE plasmalogens and increased the proportions of 18: 1 and 22:6 containing PE plasmalogens. The nominal significance of the treatment effect was determined using paired t- tests; ** indicates P < 0.01 and *** indicates P < 0.001.

[0054] FIG. 9 shows HepG2 cells before and after plasmalogen precursor treatment. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)t / 2 (AKG), LPC(O-16:0)t / 4 (LPC(O)), LPE(O-16:0)t / 5 (LPE(O)). Images were taken with an Olympus CKX41 Inverted Microscope at 4x magnification and analysed using ImageJ. Scale bar for all images is 400pm.

[0055] FIG. 10 shows labelled phosphatidylethanolamine plasmalogen (PE(P)) concentration after plasmalogen precursor treatment in HepG2 cells. FIG. 10A shows a bar chart displays of labelled PE(P) concentration of the 16:0, 18:0 and 18: 1 species. FIG. 10B shows labelled PE(P) / total label (%). Total label refers to the sum of labelled AKG, alkyl-acylglycerol (DG(O)), lysoalkylphosphatidylcholine (LPC(O)), lysophosphatidylcholine plasmalogen (LPC(P)), lysoalkylphosphatidylethanolamine (LPE(O)), lysophosphatidylethanolamine plasmalogen (LPE(P)), alkylphosphatidylcholine (PC(O)), phosphatidylcholine plasmalogen (PC(P)), alkylphosphatidylethanolamine (PE(O)), PE(P), monoalkyl-diacylglycerol (TG(O)). FIG. 10 shows mean ± standard deviation (n=3 per group) with each symbol representing an individual sample. FIG. 10B excluded control as it divides a background value by a backgroundvalue, which could be misleading. One-way ANOVA with Tukey’s post-hoc test was used, ns indicates p>0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

[0056] FIG. 11 shows label incorporation into lipid classes of the plasmalogen biosynthesis pathway after plasmalogen precursor treatment in HepG2 cells. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)t / 2 (AKG), LPC(O-16:0)t / 4 (LPC(O)), LPE(O-16:0)t / 5 (LPE(O)). Concentrations were normalised to phosphatidylcholine (PC) 34: 1, one of the most abundant endogenous PC. FIG. 11A shows a bar chart displays label concentration for AKG treatment. FIG 11B shows a bar chart displays label concentration for LPC(O) treatment. FIG. 11C shows a bar chart displays label concentration for LPE(O) treatment. FIG. 11 shows mean ± standard deviation (n=3 per group) with each symbol representing an individual sample.

[0057] FIG. 12 shows the distribution of label incorporation in the plasmalogen biosynthesis pathway after plasmalogen precursor treatment in HepG2 cells. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)d2 (AKG), LPC(O-16:0)d4 (LPC(O)), LPE(O-16:0)d5 (LPE(O)). FIG. 12A shows label concentration of each lipid class divided by total label as a percentage for AKG treatment. FIG. 12B shows label concentration of each lipid class divided by total label as a percentage for LPC(O) treatment. FIG. 12C shows label concentration of each lipid class divided by total label as a percentage for LPE(O) treatment. Total label refers to the sum of labelled AKG, alkyl-acylglycerol (DG(O)), lysoalkylphosphatidylcholine (LPC(O)), lysophosphatidylcholine plasmalogen (LPC(P)), lysoalkylphosphatidylethanolamine (LPE(O)), lysophosphatidylethanolamine plasmalogen (LPE(P)), alkylphosphatidylcholine (PC(O)), phosphatidylcholine plasmalogen (PC(P)), alkylphosphatidylethanolamine (PE(O)), phosphatidylethanolamine plasmalogen (PE(P)), monoalkyl-diacylglycerol (TG(O)).

[0058] FIG. 13 shows 3T3 cells before and after plasmalogen precursor treatment. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)d2 (AKG), LPC(O-16:0)d4 (LPC(O)), LPE(O-16:0)d5 (LPE(O)). Images were taken with an Olympus CKX41 Inverted Microscope at 4x magnification and analysed using ImageJ. Scale bar for all images is 400pm.

[0059] FIG. 14 shows labelled phosphatidylethanolamine plasmalogen (PE(P)) concentration after plasmalogen precursor treatment in 3T3 cells. Concentrations were normalisedto phosphatidylcholine (PC) 34: 1, one of the most abundant endogenous PC. FIG. 14A shows a bar chart displays of labelled PE(P) concentration of the 16:0, 18:0 and 18: 1 species. FIG. 14B shows a bar chart displaying log(2) of labelled PE(P) concentration of the 16:0, 18:0 and 18: 1 species. FIG. 14C shows labelled PE(P) / total label (%). Total label refers to the sum of labelled AKG, alkyl-acylglycerol (DG(O)), lysoalkylphosphatidylcholine (LPC(O)), lysophosphatidylcholine plasmalogen (LPC(P)), lysoalkylphosphatidylethanolamine (LPE(O)), lysophosphatidylethanolamine plasmalogen (LPE(P)), alkylphosphatidylcholine (PC(O)), phosphatidylcholine plasmalogen (PC(P)), alkylphosphatidylethanolamine (PE(O)), PE(P), monoalkyl-diacylglycerol (TG(O)). FIG. 14 shows mean ± standard deviation (n=3 per group) with each symbol representing an individual sample. FIG. 14C excluded control as it divides a background value by a background value, which could be misleading. One-way ANOVA with Tukey’s post-hoc test was used, ns indicates p>0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

[0060] FIG. 15 shows label incorporation into lipid classes of the plasmalogen biosynthesis pathway after plasmalogen precursor treatment in 3T3 cells. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)t / 2 (AKG), LPC(O-16:0)t / 4 (LPC(O)), LPE(O-16:0)t / 5 (LPE(O)). Concentrations were normalized to phosphatidylcholine (PC) 34: 1, one of the most abundant endogenous PC. FIG. 15A shows a bar chart displays label concentration for AKG treatment. FIG. 15B shows a bar chart displays label concentration for LPC(O) treatment. FIG. 15C shows a bar chart displays label concentration for LPE(O) treatment. FIG. 15 shows mean ± standard deviation (n=3 per group) with each symbol representing an individual sample.

[0061] FIG. 16 shows the distribution of label incorporation in the plasmalogen biosynthesis pathway after plasmalogen precursor treatment in 3T3 cells. Cells were treated with 0.05% ethanol (vehicle control) or labelled plasmalogen precursors at 20pM for 24 hours. Labelled precursors included alkylglycerol (O-16:0)t / 2 (AKG), LPC(O-16:0)t / 4 (LPC(O)), LPE(O-16:0)t / 5 (LPE(O)). FIG. 16A shows label concentration of each lipid class divided by total label as a percentage for AKG treatment. FIG. 16B shows label concentration of each lipid class divided by total label as a percentage for LPC(O) treatment. FIG. 16C shows label concentration of each lipid class divided by total label as a percentage for LPE(O) treatment.

[0062] FIG. 17 describes the procedure for dosing mixtures of deuterated precursor molecules on 64 eight-week-old C57BL / 6 mice.

[0063] FIG. 18 shows labelled alkylglycerol (AKG) concentration after dose mix A of plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: 1 )6 / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 18A shows a chart displaying labelled AKG 0-16:0 concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in females. FIG. 18B shows a bar chart displaying labelled AKG 0-16:0 concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in males. FIG. 18 shows mean ± standard deviation (n=4-5 per group) with each symbol representing an individual sample.

[0064] FIG. 19 shows labelled alkylphosphatidylcholine (PC(O)) concentration after dose mix A of plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O- 16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 19A shows a chart displaying labelled PC(O) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in females. FIG. 19B shows a chart displaying labelled PC(O) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in males. FIG. 19 shows mean ± standard deviation (n=4-5 per group) with each symbol representing an individual sample.

[0065] FIG. 20 shows labelled alkylphosphatidylethanolamine (PE(O)) concentration after dose mix A of plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O- 16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 20A shows a chart displaying labelled PE(O) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in females. FIG. 20B shows a chart displaying labelled PE(O) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in males. FIG. 20 shows mean ± standard deviation (n=4-5 per group) with each symbol representing an individual sample.

[0066] FIG. 21 shows labelled phosphatidylethanolamine plasmalogen (PE(P)) concentration after dose mix A of plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (O- 16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 21A shows a chart displaying labelled PE(P) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in females. FIG. 21B shows a chart displaying labelled PE(P) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix A of treatment in males. FIG. 21 shows mean ± standard deviation (n=4- 5 per group) with each symbol representing an individual sample.

[0067] FIG. 22 shows labelled phosphatidylethanolamine plasmalogen (PE(P)) concentration after dose mix B of plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (O- 16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 22A shows a chart displaying labelled PE(P) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix B of treatment in females. FIG. 22B shows a chart displaying labelled PE(P) 16:0 species concentration at 0, 1, 4, 24 and 48 timepoints for dose mix B of treatment in males. FIG. 22 shows mean ± standard deviation (n=4 per group) with each symbol representing an individual sample.

[0068] FIG. 23 shows the maximum concentration of labelled phosphatidylethanolamine plasmalogen (Cmax) after plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O-16:0)tZ5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 23A shows a bar chart displaying Cmax for dose mix A of treatment in females. FIG. 23B shows a bar chart displaying log(2) Cmax for dose mix A of treatment in females. FIG. 23C shows a bar chart displaying dose mix A of treatment in males. FIG. 23D shows a bar chart displaying log(2) Cmax dose mix A of treatment in males. FIG. 23E shows a bar chart displaying dose mix B of treatment in females. FIG. 23F shows a bar chart displaying log(2) Cmax dose mix B of treatment in females. FIG. 23G shows a bar chart displaying dose mix B oftreatment in males. FIG. 23H shows a bar chart displaying log(2) Cmax dose mix B of treatment in males. FIG. 23 shows mean ± standard deviation (n=4 per group) with each symbol representing an individual sample. One-way ANOVA with Tukey’s post-hoc test was used, ns indicates p>0.05, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

[0069] FIG. 24 shows area under the curve values for labelled phosphatidylethanolamine plasmalogen (AUC) after plasmalogen precursor treatment in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18:l)d2), LPE(O) mix (LPE(O-16:0)t / 5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 24A shows a bar chart displaying AUC for dose mix A of treatment in females. FIG. 24B shows a bar chart displaying log(2) AUC for dose mix A of treatment in females. FIG. 24C shows a bar chart displaying AUC for dose mix A of treatment in males. FIG. 24D shows a bar chart displaying log(2) AUC for dose mix A of treatment in males. FIG. 24E shows a bar chart displaying AUC for dose mix B of treatment in females. FIG. 24F shows a bar chart displaying log(2) AUC for dose mix B of treatment in females. FIG. 24G shows a bar chart displaying AUC for dose mix B of treatment in males. FIG. 24H shows a bar chart displaying log(2) AUC for dose mix B of treatment in males. FIG. 24 shows mean ± standard deviation (n=4 per group) with each symbol representing an individual sample. One-way ANOVA with Tukey’s post-hoc test was used, ns indicates p>0.05, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.

[0070] FIG. 25 shows area under the curve (AUC) for lipid classes of the plasmalogen biosynthesis pathway after dose mix A of plasmalogen precursor treatment in female mice. Eight- week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (0-16:0, 18:0, 18: 1)6 / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O- 16:0)t 5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 25A shows a bar chart displaying AUC for AKG treatment. FIG. 25B shows a bar chart displaying AUC for LPC(O) treatment. FIG. 25C shows a bar chart displaying AUC for LPE(O) treatment. FIG. 25 shows mean ± standard deviation (n=4 per group) with each symbol representing an individual sample.

[0071] FIG. 26 shows area under the curve (AUC) for lipid classes of the plasmalogen biosynthesis pathway after dose mix A of plasmalogen precursor treatment in male mice. Eight- week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix(AKG (0-16:0, 18:0, 18: l)t / 2), LPC(O) mix (LPC(O-16:0, 18:0, 18: l)t / 2), LPE(O) mix (LPE(O- 16:0)t / 5 and unlabeled LPE(O-16:0, 18:0, 18: 1)). Blood was collected through tail-tip bleeding before treatment and at 1, 4, 24 and 48 hours. FIG. 26A shows a bar chart displaying AKG treatment. FIG. 26B shows a bar chart displaying LPC(O) treatment. FIG. 26C shows a bar chart displaying LPE(O) treatment. FIG. 26 shows mean ± standard deviation (n=4 per group) with each symbol representing an individual sample.

[0072] FIG. 27 shows labelled phosphatidylethanolamine plasmalogen of the 0-16:0 species in brain after supplementation of labelled LPE(O) in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), or LPE(O) mix (LPE(O-16:0, O- 18:0, 0-18: 1, O-16:0-d5)). Brain samples were collected 48 hours after gavage. FIG. 27A shows a bar chart displaying dose mix A treatment in females. FIG. 27B shows a bar chart displaying dose mix A treatment in males. FIG. 27C shows a bar chart displaying dose mix B of treatment in females. FIG. 27D shows a bar chart displaying dose mix B of treatment in males. FIG. 27 shows mean ± standard deviation (n=4 per group), with each symbol representing an individual sample. Student’s t test was used to compare the mean differences between the groups. * p<0.05, *** p<0.001;

[0073] FIG. 28 shows labelled phosphatidylethanolamine plasmalogen of the 0-16:0 species in brain after supplementation of labelled AKG or LPC(O) in mice. Eight-week-old C57BL / 6 mice were gavaged with a single dose of lecithin (vehicle control), AKG mix (AKG (O- 16 : 0-d2, O- 18 : 0-d2, O- 18 : 1 -d2)) or LPC(O) mix (LPC(O- 16 : 0-d2, O- 18 : 0-d2. Brain samples were collected 48 hours after gavage. FIG. 28A shows a bar chart displaying dose mix A of treatment in females, FIG. 28B shows a bar chart displaying dose mix A treatment in males. FIG. 28C shows a bar chart displaying dose mix B of treatment in females. FIG. 28D shows a bar chart displaying dose mix B of treatment in males. FIG. 28 shows mean ± standard deviation (n=4 per group), with each symbol representing an individual sample. One-way ANOVA was used to test the mean differences between the groups.

[0074] FIG. 29 shows changes in the tracer alkyl diacylglycerol [TG(O)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 29A AKG-dose mix C; FIG. 29B AKD AG-oleic- dose mix C; FIG. 29C AKDAG-DHA- dose mix C; FIG. 29D LPC(O)- dose mix C; FIG. 29E AKG-dose mix D; FIG. 29F AKD AG-oleic- dose mix E; FIG. 29G AKDAG-DHA- dose mix D; FIG. 29H LPC(O)- dose mix D.

[0075] FIG. 30 shows changes in the tracer lysoalkylphosphatidylcholine [LPC(O)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 30A AKG-dose mix C; FIG. 30B AKD AG-oleic- dose mix C; FIG. 30C AKDAG-DHA- dose mix C; FIG. 30D LPC(O)- dose mix C; FIG. 30E AKG-dose mix D; FIG. 30F AKDAG- oleic- dose mix E; FIG. 30G AKDAG-DHA- dose mix D; FIG. 30H LPC(O)- dose mix D.

[0076] FIG. 31 shows changes in the tracer alkylphosphatidylcholine [PC(O)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 31A AKG-dose mix C; FIG. 31B AKD AG-oleic- dose mix C; FIG. 31C AKDAG-DHA- dose mix C; FIG. 31D LPC(O)- dose mix C; FIG. 31E AKG-dose mix D; FIG. 31F AKDAG- oleic- dose mix E; FIG. 31G AKDAG-DHA- dose mix D; FIG. 31H LPC(O)- dose mix D.

[0077] FIG. 32 shows changes in the tracer alkylphosphatidylethanolamine [PE(O)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 32A AKG-dose mix C; FIG. 32B AKD AG-oleic- dose mix C; FIG. 32C AKDAG-DHA- dose mix C; FIG. 32D LPC(O)- dose mix C; FIG. 32E AKG-dose mix D; FIG. 32F AKDAG- oleic- dose mix E; FIG. 32G AKDAG-DHA- dose mix D; FIG. 32H LPC(O)- dose mix D.

[0078] FIG. 33 shows changes in the tracer alkenylphosphoethanolamine [PE(P)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 33A AKG-dose mix C; FIG. 33B AKD AG-oleic- dose mix C; FIG. 33C AKDAG-DHA- dose mix C; FIG. 33D LPC(O)- dose mix C; FIG. 33E AKG-dose mix D; FIG. 33F AKDAG- oleic- dose mix E; FIG. 33G AKDAG-DHA- dose mix D; FIG. 33H LPC(O)- dose mix D.

[0079] FIG. 34 shows changes in the tracer alkenylphosphatidylcholine [PC(P)] concentration following administration of different precursor compounds. Precursor compounds are FIG. 34A AKG-dose mix C; FIG. 34B AKD AG-oleic- dose mix C; FIG. 34C AKDAG-DHA- dose mix C; FIG. 34D LPC(O)- dose mix C; FIG. 34E AKG-dose mix D; FIG. 34F AKDAG- oleic- dose mix E; FIG. 34G AKDAG-DHA- dose mix D; FIG. 34H LPC(O)- dose mix D.

[0080] FIG. 35 shows Maximum plasma concentration (Cmax) of major lipid classes following administration of different precursor compounds. Precursor compounds are FIG. 35A TG(O); FIG. 35B LPC(O); FIG. 35C PC(O); FIG. 35D PE(O); FIG. 35E PE(P); FIG. 35F PC(P).

[0081] FIG. 36 shows Area under the curve (AUC) of major lipid classes following administration of precursor compounds. Precursor compounds are FIG. 36A TG(O); FIG. 36B LPC(O); FIG. 36C PC(O); FIG. 36D PE(O); FIG. 36E PE(P); FIG. 36F PC(P).

[0082] FIG. 37 shows the effect of labelled precursor supplementation on the major ether lipids classes in liver. Precursor compounds are FIG. 37A TG(O); FIG. 37B LPC(O); FIG. 37C PC(O); FIG. 37D PE(O); FIG. 37E PE(P); FIG. 37F PC(P).

[0083] FIG. 38 shows the effect of labelled precursor supplementation on the major ether lipids classes in spleen. Precursor compounds are FIG. 38A TG(O); FIG. 38B LPC(O); FIG. 38C PC(O); FIG. 38D PE(O); FIG. 38E PE(P); FIG. 38F PC(P).

[0084] FIG. 39 shows the effect of labelled precursor supplementation on the major ether lipids classes in brain. Precursor compounds are FIG. 39A TG(O); FIG. 39B LPC(O); FIG. 39C PC(O); FIG. 39D PE(O); FIG. 39E PE(P); FIG. 39F PC(P).

[0085] FIG. 40 shows the effect of labelled precursor supplementation on the major ether lipids classes in kidney. Precursor compounds are FIG. 40A TG(O); FIG. 40B LPC(O); FIG. 40C PC(O); FIG. 40D PE(O); FIG. 40E PE(P); FIG. 40F PC(P).

[0086] FIG. 41 shows the effect of labelled precursor supplementation on the major ether lipids classes in visceral adipose tissue. Precursor compounds are FIG. 41A TG(O); FIG. 41B LPC(O); FIG. 41C PC(O); FIG. 41D PE(O); FIG. 41E PE(P); FIG. 41F PC(P).

[0087] FIG. 42 shows the effect of labelled precursor supplementation on the major ether lipids classes in skeletal muscle. Precursor compounds are FIG. 42A TG(O); FIG. 42B LPC(O); FIG. 42C PC(O); FIG. 42D PE(O); FIG. 42E PE(P); FIG. 42F PC(P).

[0088] FIG. 43 shows the effect of labelled precursor supplementation on the major ether lipids classes in heart. Precursor compounds are FIG. 43A TG(O); FIG. 43B LPC(O); FIG. 43C PC(O); FIG. 43D PE(O); FIG. 43E PE(P); FIG. 43F PC(P).

[0089] FIG. 44 shows the effect of LPC(O) supplementation on plasmalogen level in RAW 264.7 cells. RAW 264.7 macrophages cells were treated with 20 pM of LPC(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The PE plasmalogen or PE(P) data are normalised to total cellular phosphatidylcholine (PC) level and presented as mean±SD (n=3 / group). Each circle represents individual data point. Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test. *indicates P<0.05, **indicates P<0.01 and **** indicates P<0.0001 vs control.

[0090] FIG. 45 shows the effect of LPE(O) supplementation on plasmalogen level in RAW 264.7 cells. RAW 264.7 macrophages cells were treated with 20 pM of LPE(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The PE plasmalogen or PE(P) 1data are normalised to total cellular phosphatidylcholine (PC) level and presented as mean±SD (n=3 / group). Each circle represents individual data point. Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test. **** indicates P<0.0001 vs control.

[0091] FIG. 46 shows the effect of LPC(O) supplementation on plasmalogen composition in RAW 264.7 cells. RAW 264.7 macrophages cells were treated with 20 pM of LPC(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The relative proportions of different SN1 containing PE(P)s are presented as mean±SD (n=3 / group).

[0092] FIG. 47 shows the effect of LPC(O) supplementation on plasmalogen level in 3T3-L1 cells. 3T3-L1 pre-adipocyte cells were treated with 20 pM of LPC(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The PE plasmalogen or PE(P) data are normalised to total cellular phosphatidylcholine (PC) level and presented as mean±SD (n=3 / group). Each circle represents individual data point. Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test, indicates P<0.05, **indicates P<0.01 and **** indicates P<0.0001 vs control.

[0093] FIG. 48 shows the effects of LPE(O) supplementation on plasmalogen level in 3T3-L1 cells. 3T3-L1 pre-adipocyte cells were treated with 20 pM of LPE(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The PE plasmalogen or PE(P) data are normalised to total cellular phosphatidylcholine (PC) level and are presented as mean±SD (n=3 / group). Each circle represents individual data point. Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test, indicates P<0.05, **indicates P<0.01, ***indicates P<0.001 and **** indicates P<0.0001 vs control.

[0094] FIG. 49 shows the effects of LPC(O) supplementation on plasmalogen composition in 3T3-L1 cells. 3T3-L1 cells were treated with 20 pM of LPC(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The relative proportions of different SN1 containing PE(P) are presented as mean±SD (n=3 / group).

[0095] FIG. 50 shows the effects of LPE(O) supplementation on plasmalogen composition in 3T3-L1 cells. 3T3-L1 cells were treated with 20 pM of LPE(O) with different SN1 compositions for 24 hours and then harvested for lipidomic analysis. The relative proportions of different SN1 containing PE(P) are presented as mean±SD (n=3 / group).

[0096] FIG. 51 shows the label incorporation (Area under the curve) into lipid classes of the plasmalogen biosynthesis pathway after low dose of plasmalogen precursor supplementation. FIG. 51A shows incorporation following AKG supplementation; FIG. 51B shows incorporation following AKD AG-oleic supplementation; FIG. 51C shows incorporation following AKDAG- DHA supplementation; FIG. 51D shows incorporation following LPC(O) supplementation.

[0097] FIG. 52 shows the % distribution of label incorporation in the plasmalogen biosynthesis pathway after plasmalogen precursor supplementation. FIG. 52A shows incorporation following AKG supplementation; FIG. 52B shows incorporation following AKDAG-oleic supplementation; FIG. 52C shows incorporation following AKDAG-DHA supplementation; FIG. 52D shows incorporation following LPC(O) supplementation.

[0098] FIG. 53 shows the labelled ether lipids in feces after 24 hours of labelled precursor supplementation FIG. 53A TG(O); FIG. 53B LPC(O); FIG. 53C PC(O); FIG. 53D PE(O); FIG. 53E PE(P); FIG. 53F PC(P).

[0099] FIG. 54 shows the labelled ether lipids in feces after 24 hours of labelled precursor supplementation FIG. 54A TG(O); FIG. 54B LPC(O); FIG. 54C PC(O); FIG. 54D PE(O); FIG. 54E PE(P); FIG. 54F PC(P).[000100] FIG. 55 shows all of the LPX(O) treatments suppressed the LPS-induced increase in TLR4 gene expression. Data are normalized to control + LPS. Data are presented as mean ± SD (n=3 / group). Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test. An asterisk (*) indicates P<0.05 vs control, indicates P<0.05 vs control+LPS.[000101] FIG. 56 shows all of the LPX(O) treatments suppressed the LPS-induced increase in TLR4 gene expression. Data are normalized to control. Data are presented as mean ± SD (n=3 / group). Mean difference between the groups were compared by one-way ANOVA followed by Fishers LSD test, indicates P<0.05 vs control, indicates P<0.05 vs control+LPS.[000102] FIGs. 57A-C show the effect of alkylglycerol supplementation on amylin diet induced model of non-alcoholic fatty liver disease in mice. The bar plots represent fat mass (FIG. 57A), liver triglyceride (TG) (FIG. 57B) at 4, 12 and 24 weeks, and gene expression (FIG. 57C; relative to Chow group) at 24-week time point. Each time point represents an independent study. Data presented as mean±SEM, n=8-13 / group. Two-way ANOVA with Fisher’s LSD post-hoc test was used to assess significance (indicates p<0.05 vs Chow and*indicates p<0.05 vs Amylin groups). Cptla: Carnitine Palmitoyl-TransferaselA; Acoxl : Peroxisomal acyl-coenzyme A oxidase 1; Tnfa: Tumour necrosis factor alpha; Collal : Collagen type I alpha 1.[000103] FIG. 58 Experimental plan to study the effect of LPX(O) supplementation in amylin diet induced model of NAFLD in mice.[000104] FIG. 59. Demonstrates the effects of plasmalogen precursor supplementation on food intake in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group. Y-axis is g / mouse / day.[000105] FIG. 60. Shows the effects of plasmalogen precursor supplementation on body mass in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. No statistically significant differences were detected between groups by one-way ANOVA.[000106] FIG. 61. Illustrates the effects of plasmalogen precursor supplementation on the area under the curve (AUC) for plasma PE(P) levels over eight weeks of chow diet feeding supplemented with different plasmalogen precursors. Data are presented as mean ± SEM (n = 5- 7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio, PE(P): alkenylphosphatidylethanolamine. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000107] FIG. 62. Shows the effects of plasmalogen precursor supplementation on serum PE(P) level in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio, PE(P): alkenylphosphatidylethanolamine. One-wayANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000108] FIG. 63. Exemplifies the effects of plasmalogen precursor supplementation on serum PE(O) level in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio, PE(O): alkylphosphatidylethanolamine. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000109] FIG. 64. Demonstrates the effects of plasmalogen precursor supplementation on liver PE(P) level in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio, PE(P): alkenylphosphatidylethanolamine. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000110] FIG. 65. Illustrates the effects of plasmalogen precursor supplementation on liver PE(O) level in mice fed with chow diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 5-7 / group). AKG, alkylglycerol; LPC(O): lysoalkylphosphatidylcholine, LPE(O), lysoalkylphosphatidylethanolamine, PE(O): alkylphosphatidylethanolamine. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000111] FIG. 66. Shows the effects of plasmalogen precursor supplementation on food intake in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assessdifferences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000112] FIG. 67. Illustrates the effects of plasmalogen precursor supplementation on body mass in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio.One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000113] FIG. 68. Shows effects of plasmalogen precursor supplementation on fat mass in mice fed diets supplemented with different plasmalogen precursors for eight weeks.Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.FIG. 69. Effects of plasmalogen precursor supplementation on lean mass in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000114] FIG. 70. Demonstrates the effects of plasmalogen precursor supplementation on liver mass in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol;LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000115] FIG. 71. Effects of plasmalogen precursor supplementation on visceral adipose tissue mass in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000116] FIG. 72. Shows the effects of plasmalogen precursor supplementation on serum PE(P) level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; PE(P): alkenylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000117] FIG. 73. Effects of plasmalogen precursor supplementation on serum cholesterol level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000118] FIG. 74. Shows the effects of plasmalogen precursor supplementation on liver triglyceride level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group.[000119] FIG. 75. Effects of plasmalogen precursor supplementation on liver PE(P) level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data arepresented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; PE(P): alkenylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. No statistically significant differences were detected between groups by one-way ANOVA.[000120] FIG. 76. Illustrates the effects of plasmalogen precursor supplementation on liver cardiolipin level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; AKG, alkylglycerol; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000121] FIG. 77. Effects of plasmalogen precursor supplementation on serum glucose level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000122] FIG 78. Effects of plasmalogen precursor supplementation on serum insulin level in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000123] FIG 79. Effects of plasmalogen precursor supplementation on HOMA-IR score in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are presented as mean ± SEM (n = 10 / group). HFD, high-fat diet; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differencesbetween group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000124] FIG. 80. Effects of plasmalogen precursor supplementation on liver insulin receptor substrate 2 (Irs2) gene expression in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are normalised to hypoxanthine-guanine phosphoribosyltransferase Hprf) gene expression and presented as mean ± SEM (n = 10 / group), relative to the Chow control group. HFD, high-fat diet; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000125] FIG. 81. Effects of plasmalogen precursor supplementation on liver glucose-6- phosphatase catalytic subunit (G6pc) gene expression in mice fed diets supplemented with different plasmalogen precursors for eight weeks. Data are normalised to hypoxanthine-guanine phosphoribosyltransferase Hprf) gene expression and presented as mean ± SEM (n = 10 / group), relative to the Chow control group. HFD, high-fat diet; LPE(O), lysoalkylphosphatidylethanolamine; mix, a combination of 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. One-way ANOVA followed by Fisher’s LSD post hoc test was used to assess differences between group means; * indicates p<0.05 compared to the Chow control group,Aindicates p<0.05 compared to the HFD control group.[000126] FIGs. 82 A-G show study design and results of plasmalogen precursor supplementation to attenuate cardiac pathology and sustain heart function in a setting of heart failure. FIG. 82A shows study design; FIG. 82B PC(P) and PE(P) species in the ventricles groups were compared by two way ANOVA with Sidak's multiple comparison's test; FIG. 82C PC(P) and PE(P) species in the plasma groups were compared by two way ANOVA with Sidak's multiple comparison's test; FIG. 82D Heart weight / tibia length (HW / TL), Lung weight / TL (LW / TL) and Kidney weight / TL (KIDW / TL) changes with diet groups were compared by two way ANOVA with Tukey’s post hoc analysis test; FIG. 82E Heart fibrosis in DCM mice on a chow diet compared to non-transgenic mice (NTg) groups were compared by two way ANOVA with Tukey’s post hoc analysis test; FIG. 82F Changes in ejection fraction between BL and EP in DCM and NTg mice groups were compared paired T-test; FIG. 82G Changes in cardiac stressmarkers (Nppb; Col3al; Atp2a2; and Ppargcla) between DCM and NTg hearts groups were compared by two way ANOVA with Tukey’s post hoc analysis test.[000127] FIGs. 83A Study design and results of plasmalogen precursor supplementation; FIG. 83B Analysis of circulating proinflammatory monocytes in a setting of ischemia reperfusion injury groups were compared by two way ANOVA with Tukey’s post hoc analysis test.[000128] FIG. 84 Study design to assess the protective effects of plasmalogen precursor supplementation in a settings of a heart attack.[000129] FIG. 85 Study design to assess the protective effects of plasmalogen precursor supplementation from recurring heart attacks.[000130] FIG. 86 Demonstration of increased PE(P) in immortalised H9C2 rat cardiomyoblasts incubated with LPE(O) or AKG ether lipids in 2D cell cultures. Lipid concentrations were normalised to phosphatidylethanolamine (PE) levels. Bars represent mean ± SD, with individual data points shown. One-way ANOVA with Tukey’s correction for multiple comparisons was performed. **: p<0.01; ***: p<0.001; ****: p<0.0001.[000131] FIG. 87 Demonstration of (A) increased PE(P) and (B) cardiolipin in iPSC- derived human cardiomyoblasts incubated with LPE(O) or AKG ether lipids. Lipid concentrations were normalised to PE levels. Bars represent mean ± SD, with individual data points shown. One-way ANOVA with Tukey’s correction for multiple comparisons was performed, ns: p>0.05; *: p<0.05; ****: p<0.0001.[000132] FIG. 88 Illustration of levels of (A) PE(O) and (B) PE plasmalogen following precursor pre-treatment + / - 1 hr H2O2 injury of 3D iPSC-derived cardiomyocyte spheroids. Lipid concentrations were normalised to PE levels. Bars represent mean ± SD, with individual data points shown. One-way ANOVA with Tukey’s correction for multiple comparisons was performed, ns: p>0.05; *: p<0.05; **: p<0.01***: p<0.001; ****: p<0.0001.[000133] FIG. 89 (A) Mitochondrial reactive oxygen species, (B) Beats per minute and (C) Systole / diastole ratio as analysed from contractile function assessed in 3D iPSC-derived cardiomyocyte spheroids following 20 pM LPE(O) pre-treatment + / - 1 hr H2O2 injury. Data were normalised to matched controls. Bars represent mean ± SD, with individual data points shown. One-way ANOVA with Tukey’s correction for multiple comparisons was performed. *: p<0.05; **: p<0.01; ***: p<0.001; ****: p<0.0001.[000134] FIG. 90A shows a diagram depicting an experimental design to study the effects of labelled plasmalogen precursor supplementation to mothers on mother’s milk and pup’s circulatory / tissue plasmalogens.[000135] FIG. 90B shows a diagram depicting an experimental design to study the effects of chronic plasmalogen precursor supplementation to mothers on mother’s milk and pup’s circulatory / tissue plasmalogens.[000136] FIG. 90C shows a diagram depicting an experimental design to study the role of breast milk ether lipids in enhancing immune responses.[000137] FIG. 90D shows a diagram depicting an experimental design to study the role of breast milk ether lipids in protecting against pathogenic inflammation.[000138] FIG. 91 shows the functional output of an MS model in vivo mouse study (A) Mouse body weight measurements for MS model study and (B) EAE scoring for MS model study[000139] FIG. 92 shows basic MEA data, compared to medium as vehicle control at 11 and 14 div. Shown are Spike rate (top) and number of units representing active neurons (bottom). Mean ± standard error. Student’s unpaired t-test vs. control (* / ** / ***)with p < 0.05 / 0.01 / 0.001.[000140] FIG. 93 MEA Burst amplitude data for MPP+ PD model at 21 DIV. From left to right: Vehicle, Vehicle +MPP (20 pM), MPP+ GDNF (20 ng / ml), MPP+LPE(O) 2 pM, MPP+ LPE(O) 5 pM, MPP+ LPE(O) 10 pM.[000141] FIG. 94 Prediction of the culture age of chronically treated frontal cortex cultures using an artificial neuronal network algorithm - Early Brain Development Index. Left panel, unsubtracted data. Right panel, vehicle control subtracted data. At each DIV the bars represent from left to right, medium control, BDNF (20 ng / ml), DHA (20 pM), LPE(O) (5 pM), LPE(O) + DHA (5 pM | 20 pM). Mean ± standard error. Student’s unpaired t-test vs. control.[000142] FIG. 95 (A) depicts an experimental overview for neurodegenerative assays. Cells are prepared, and passaged at 70-80% confluency prior to shorthairpin (sh) RNA induction and differentiation. The shRNA is designed to target FAR1 mRNA to knockdown translation into protein. Seeding level is dependent upon experiment. FIG. 95 (B) Imaging Procedure for Scratch Assay[000143] FIG. 96. Quantitative lipidomics data obtained from differentiated SH-SY5Y neuroblastoma cells showing total lipid class abundance of (A) diacyl PE and (B) ether PE / (PE(O)) following treatment with 20 pM plasmalogen precursors for 15-days. LPE(O) treatmentproduces 2.36x increase in ether PEs as compared to Vehicle. Statistics obtained by one-way ANOVA with Bonferroni correction. ** denotes p< 01 . *** denotes p< 001 .[000144] Table 1 The list of abbreviations used in this disclosure.Table 1zsZellweger SyndromeDETAILED DESCRIPTION[000145] The general structure of the phospholipids described herein is depicted by the following Formula (I):(I).[000146] In compounds of Formula (I), the sn-1 carbon is labeled as above. R3includes phosphate and substituted phosphate. R1and R2can each be independently hydrogen, alkyl, alkenyl, acyl or the like, or substituted versions of these moieties as described herein.[000147] In Scheme I, some typical plasmalogens are shown in the top two structures, the boxes highlighting the sn-1 substitution as derived from Formula (I).Scheme I. Typical plasmalogens and related glycerophospholipids[000148] Definitions[000149] Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by those of ordinary skill in the art to which the disclosure belongs.[000150] The term "and / or", e.g., "X and / or Y" shall be understood to mean "X and Y" or "X or Y" and shall be taken to provide explicit support for both meanings or for either meaning.[000151] The terms “a” and “an” as used herein mean “one or more” and include the plural unless the context is inappropriate. The use of singular articles in the context of describing the present disclosure (especially in the context of the claims) are to be construed to cover both the singular and the plural, unless otherwise indicated herein or clearly contradicted by context. Recitation of ranges of values herein are merely intended to serve as a shorthand method of referring individually to each separate value falling within the range, unless otherwise indicated herein, and each separate value is incorporated into the specification as if it were individually recited herein.[000152] Use of the term “about” is intended to describe values either above or below the stated value in a range of approximately ±10%; in other embodiments, the values may range in value above or below the stated value in a range of approximately ±5%; in other embodiments, the values may range in value above or below the stated value in a range of approximately ±2%; in other embodiments, the values may range in value above or below the stated value in a range of approximately ±1%. The preceding ranges are intended to be made clear by context, and no further limitation is implied. All methods described herein can be performed in any suitable order unless otherwise indicated herein or otherwise clearly contradicted by context.[000153] As used herein the term “body mass index” is used interchangeably with “BMI” and refers to a weight-to-height ratio calculated by dividing a subject’s weight in kilograms by the square of the subject’s height in meters. A BMI below 18.5 is underweight. A BMI between 18.5- 24.9 is normal weight. A BMI of 25.0-29.9 is overweight. A BMI over 30 is obese, and includes class I (30.0-34.9), class II (35.0-39.9), and class III (>40).[000154] As used herein the term “overweight” refers to a subject with a body mass index between 25 and 29.9. A person may also be diagnosed as overweight by other measures including waist circumference or body composition analysis.[000155] As used herein the term “obese” refers to a subject with a body mass index greater than 30. A person may also be diagnosed as obese by other measures including waist circumference or body composition analysis.[000156] As used herein the term “liver disease” can be used interchangeably with “hepatic disease” and includes “chronic liver diseases.” Liver diseases have common features such ashepatic steatosis, hepatitis, fibrosis, and cirrhosis. Hepatic steatosis is characterized by an accumulation of fat in the liver. Hepatitis is inflammation of the liver tissue. Liver fibrosis is the replacement of functional liver tissue with fibrous scar tissue. Cirrhosis occurs when liver function becomes impaired, generally because of extensive liver fibrosis. Liver cirrhosis is most commonly associated with NAFLD progressing to NASH, which most commonly occurs in subjects with other comorbidities such as: obesity, high blood pressure, abnormal levels of cholesterol, type 2 diabetes, and metabolic syndrome. Cirrhosis can also be associated with autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, and genetic disorders such as Wilson’s disease, hereditary hemochromatosis and chronic heart failure with liver congestion.[000157] As used herein the term, “Non-alcoholic fatty liver disease” is used interchangeably with the abbreviation “NAFLD” and the term “metabolic dysfunction-associated steatotic liver disease” s used interchangeably with the abbreviation “MASLD”. NAFLD is early-stage liver disease associated with excessive fat build-up in the liver in which liver function remains largely intact. NAFLD can progress to NASH.[000158] As used herein the term “non-alcoholic steatohepatitis” (NASH) can be used interchangeably with “metabolic-associated steatohepatitis” (MASH). NASH is characterized by inflammation, progressive replacement of healthy liver with fibrosis, and cirrhosis. NASH is associated with obesity, high blood pressure, abnormal levels of cholesterol, type 2 diabetes, and metabolic syndrome. NASH is also associated with development of liver cancer (e.g., hepatocellular carcinoma).[000159] As used herein, and as well understood in the art, “to treat” a condition or “treatment” of the condition (e.g., the conditions described herein such as liver disease) is an approach for obtaining beneficial or desired results, such as clinical results. Beneficial or desired results can include, but are not limited to, alleviation or amelioration of one or more symptoms or conditions; diminishment of extent of disease, disorder, or condition; stabilized (i.e., not worsening) state of disease, disorder, or condition; preventing progression of disease, disorder, or condition; delay or slowing the progress of the disease, disorder, or condition; amelioration or palliation of the disease, disorder, or condition; and reversal of the disease, disorder, or condition (whether partial or total), whether detectable or undetectable. “Palliating” a disease, disorder, or condition means that the extent and / or undesirable clinical manifestations of the disease,disorder, or condition are lessened and / or time course of the progression is slowed or lengthened, as compared to the extent or time course in the absence of treatment.[000160] As used herein, the term “to prevent” or “prevention” may be used interchangeably with “prophylactic treatment,” “protection from,” “prevention of liver disease,” and as used herein the term means administering LPX(O)s and plasmalogen precursors to a subject to prevent the development or progression of liver disease (i.e. progression from NAFLD to NASH). Prophylactic treatment to prevent liver disease may also include treating a patient suspected of developing liver disease based on clinical prognostic features (e.g. obesity). Prophylactic treatment preserves liver function by reversing, reducing, or preventing liver disease including markers of steatosis, liver inflammation, liver fibrosis, and cirrhosis. Prophylactic treatment may be fixed or may be individualized to compensate for subject-to- subject clinical variability.[000161] The term “alkyl” as used herein refers to a saturated straight or branched hydrocarbon, such as a straight or branched group of 1-30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci-Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively. Exemplary alkyl groups include, but are not limited to, methyl, ethyl, propyl, butyl, pentyl, hexyl, heptyl, octyl, nonyl, decyl, undecyl, dodecyl, tridecyl, tetradecyl, pentadecyl, hexadecyl, heptadecyl, octadecyl, isopropyl, 2 -methyl- 1 -propyl, 2-methyl-2-propyl, 2-methyl-l- butyl, 3 -methyl- 1 -butyl, 2-methyl-3 -butyl, 2,2-dimethyl-l -propyl, 2 -m ethyl- 1 -pentyl, 3 -methyl- 1- pentyl, 4-m ethyl- 1 -pentyl, 2-methyl-2-pentyl, 3-methyl-2-pentyl, 4-methyl-2-pentyl, 2,2- dimethyl-l -butyl, 3, 3 -dimethyl- 1 -butyl, 2-ethyl-l -butyl, isobutyl, t-butyl, isopentyl, neopentyl, etc.[000162] The term “alkenyl” as used herein refers to an unsaturated straight or branched hydrocarbon, such as a straight or branched group of 2-30, 2-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4-C24alkenyl Cw-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively. Multiple double bonds may be present in an alkenyl compound. Exemplary alkenyl groups include, but are not limited to, ethenyl, propenyl, butenyl, pentenyl, hexenyl, heptenyl, octenyl, nonenyl, decenyl, undecenyl, dodecenyl, tridecenyl, tetradecenyl, pentadecenyl, hexadecenyl, heptadecenyl, octadecenyl, isopropenyl, 2-methyl-l- butenyl, 3 -methyl- 1 -butenyl, 2-methyl-3 -butenyl, 2,2-dimethyl-l -propenyl, 2-methyl-l -pentenyl, 3 -methyl- 1 -pentenyl, 4-methyl-l -pentenyl, 2-methyl-2-pentenyl, 3-methyl-2-pentenyl, 4-m ethyl-2-pentenyl, 2,2-dimethyl-l-butenyl, 3, 3 -dimethyl- 1-butenyl, 2-ethyl-l-butenyl, isobutenyl, t- butenyl, isopentenyl, neopentenyl, etc. The term “alkenyl” can additionally be taken to mean an alkene of structure Cl 8: 1 wherein the double bond is typically at the n7 or n9 position. The term “alkenyl” can additionally be taken to mean an alkene of structure Cl 8: 1 wherein the double bond is between the first and second carbon adjacent to the ether link. The term “alkenyl” can additionally be taken to mean an alkene wherein one double bond is at the n7 or n9 position and a second double bond is between the first and second carbon.[000163] The term “acyl” as used herein refers to a radical of general formula -C(O)R, wherein R is hydrogen or a saturated or unsaturated straight or branched hydrocarbon, such as a straight or branched group of 1-30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci-Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively or a straight or branched group of 2-30, 2-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4-C24alkenyl Cu-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively. Exemplary alkyl groups include, but are not limited to, methyl, ethyl, propyl, butyl, pentyl, hexyl, heptyl, octyl, nonyl, decyl, undecyl, dodecyl, tridecyl, tetradecyl, pentadecyl, hexadecyl, heptadecyl, octadecyl, isopropyl, 2 -methyl- 1 -propyl, 2-methyl-2-propyl, 2-methyl-l- butyl, 3 -methyl- 1 -butyl, 2-methyl-3 -butyl, 2,2-dimethyl-l -propyl, 2 -m ethyl- 1 -pentyl, 3 -methyl- 1- pentyl, 4-m ethyl- 1 -pentyl, 2-methyl-2-pentyl, 3-methyl-2-pentyl, 4-methyl-2-pentyl, 2,2- dimethyl-l -butyl, 3, 3 -dimethyl- 1 -butyl, 2-ethyl-l -butyl, isobutyl, t-butyl, isopentyl, neopentyl, etc.[000164] The term “ether” as used herein, refers to any organic compound with a structure similar to an ether functional group, having an oxygen atom linking two alkyl or other organic groups. As used herein, the term “ether” may refer to a functional group, having an oxygen atom linking a saturated straight or branched hydrocarbon, such as a straight or branched group of 1- 30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci-Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively and a second saturated straight or branched hydrocarbon. As used herein, the term “ether” may also refer to a functional group, having an oxygen atom linking a saturated straight or branched hydrocarbon, such as a straight or branched group of 1-30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci- Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively and an unsaturated straight or branched hydrocarbon such as a straight or branched group of 2-30, 2-18,14-24, 14-18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4- C24alkenyl Cu-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively. As used herein, the term “ether” may also refer to a functional group, having an oxygen atom linking an unsaturated straight or branched hydrocarbon, such as a straight or branched group of 2-30, 2-18, 14-24, 14- 18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4-C24alkenyl Ci4-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively, and a second unsaturated straight or branched hydrocarbon.[000165] As used herein, the term “vinyl ether” refers to a group wherein an alkene is adjacent to an ether linkage.[000166] The term “ester” as used herein, refers to any organic compound with a structure similar to an ester functional group. As referred to herein, the term “ester” refers to any compound or functional group that can be represented by a radical of general formula -RCOOR’, wherein R is hydrogen or a saturated or unsaturated straight or branched hydrocarbon, such as a straight or branched group of 1-30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci-Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively or a straight or branched group of 2-30, 2-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4-C24alkenyl Cu-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively, and R’ is a saturated or unsaturated straight or branched hydrocarbon, such as a straight or branched group of 1-30, 1-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as Ci-Csoalkyl, Ci-Cisalkyl, Ci4-C24alkyl Cu-Cisalkyl, Ciealkyl, or Cisalkyl respectively or a straight or branched group of 2-30, 2-18, 14-24, 14-18, 16 or 18 carbon atoms, referred to herein as C2-C3oalkenyl, C2-Cisalkenyl, Ci4-C24alkenyl Cu-Cisalkenyl, Ciealkenyl, or Cisalkenyl respectively.[000167] The terms “substituted” and “optionally substituted” in reference to phosphate groups, alkyl groups, alkenyl groups, or acyl groups refers to the optional substitution of these groups by an additional moiety. In each case, the substituent or additional moiety may be independently selected from hydrogen, Ciealkyl, and halogen (e.g., Cl, F, Br or I). In certain embodiments, the group is not substituted, i.e., it is unsubstituted.[000168] The naming convention for lipids used here follows the guidelines established by the Lipid Maps Consortium and the shorthand notation of Liebisch et al. (Liebisch et al., Fahy et. al. (2009), Fahy et al. (2005)]. Alternatively, the nomenclature is based on BiochemicalNomenclature and Related Documents, 2nd edition, Portland Press (London, 1992) Edited C Liebecq. [ISBN 1-85578-005-4], “Nomenclature of Lipids.” Phospholipids typically contain two fatty acid chains and in the absence of detailed characterization are expressed as the sum composition of carbon atoms and double bonds (e.g. PC(38:6)). However, where an acyl chain composition has been determined the naming convention indicates this (e.g. PC(38:6) is changed to PC(16:0 / 22:6)).[000169] The present disclosure refers to lipid molecules using the numbering system X:Y. The number X represents the number of carbon atoms present in the chain.[000170] In the context of alkylglycerols, alkylacylglycerols, and alkyldiacylglycerols, the number Y represents the number of double bonds present in the chain. For example, an alkylglycerol numbered as 16:0 contains a hydrocarbon group having a 16-carbon chain with no double bonds. As a further example, an alkylglycerol numbered as 18: 1 contains a hydrocarbon group having an 18-carbon chain with 1 double bond.[000171] In the context of plasmalogens / plasmenyl phospholipids, the number Y in the first listed alkenyl chain (i.e. PE(P-X:Y / X:Y) represents the number of double bonds present in the alkenyl chain in addition to the vinyl ether group. For example, in a plasmalogen numbered as PE(P-16:0 / 20:4) the 16:0 alkenyl group contains a hydrocarbon group having a 16-carbon chain with no double bonds other than the vinyl ether group (i.e., there is a double bond between the first 2 carbons and the remaining 14 carbons are saturated). As another example, in a plasmalogen numbered as PE(P-18: 1 / 20:4), the 18: 1 alkenyl group contains a hydrocarbon group having an 18- carbon chain with 1 double bond in addition to the vinyl ether group (i.e., there is a double bond between the first 2 carbon atoms, and there is one other double bond between 2 carbons out of the remaining 16 carbons). As shown above in Scheme I, the plasmenyl PE plasmalogen is represented by the structure PE(P-16:0 / 22:6).[000172] Where ether lipids contain one or more double bonds, the double bonds may be located at various positions in the hydrocarbon chains. For example, an alkylglycerol numbered as 18: 1 may contain a mixture of species, e.g. with cv.s-n l and cis-rD double bonds. As another example, a plasmalogen (e.g., PE(P)) numbered as 18: 1 may contain a mixture of species, e.g., with cv.s-n l and cis-rD double bonds.[000173] As used herein, the term “plasmanyl” shall be understood to refer to phospholipids having an ether bond in the sn-1 position to an alkyl group.[000174] As used herein, the term “plasmenyl” shall be understood to refer to phospholipids having an ether bond in the sn-1 position to an alkenyl group. The plasmenyl phospholipids are referred to as “plasmalogens”.[000175] A plasmalogen having a “15:0” alkenyl group is a molecule having an ether bond in the sn-1 position to a 15-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and no other double bonds in the chain.[000176] A plasmalogen having a “16:0” alkenyl group is a molecule having an ether bond in the sn-1 position to a 16-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and no other double bonds in the chain.[000177] A plasmalogen having a “17:0” alkenyl group is a molecule having an ether bond in the sn-1 position to a 17-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and no other double bonds in the chain.[000178] A plasmalogen having an “18:0” alkenyl group is a molecule having an ether bond in the sn-1 position to an 18-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and no other double bonds in the chain.[000179] A plasmalogen having an “18: 1” alkenyl group is a molecule having an ether bond in the sn-1 position to an 18-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and having one additional double bond, typically between carbons 7 and 8 (e.g., n7), between carbons 9 and 10 e.g., n9), or between carbons 11 and 12 (e.g., n i l), and typically a c / .s-double bond.[000180] A plasmalogen having a “20:0” alkenyl group is a molecule having an ether bond in the sn-1 position to a 20-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and no other double bonds in the chain.[000181] A plasmalogen having an “20: 1” alkenyl group is a molecule having an ether bond in the sn-1 position to a 20-carbon chain which contains a double bond between carbons 1 and 2 (typically a c / .s- vinyl ether group), and having one additional double bond, typically between carbons 7 and 8 or between carbons 9 and 10, and typically a c / .s-double bond.[000182] A plasmalogen having an “18:2” acyl alkenyl group is a molecule having an ester bond in the sn-2 position to an 18-carbon chain which has two double bonds, typically between carbons 9 and 10, and between carbons 11 and 12, and typically c / .s-double bonds.[000183] A plasmalogen having a “20:4” acyl alkenyl group is a molecule having an ester bond in the sn-2 position to a 20-carbon chain which has four double bonds, typically between carbons 5 and 6, carbons 8 and 9, carbons 11 and 12, and carbons 14 and 15, and typically cisdouble bonds.[000184] A plasmalogen having a “22:6” acyl alkenyl group is a molecule having an ester bond in the sn-2 position to a 22-carbon chain which has six double bonds, typically between carbons 4 and 5, carbons 7 and 8, carbons 10 and 11, carbons 13 and 14, carbons 16 and 17, and carbons 19 and 20, and typically c / .s-double bonds.[000185] The term “plasmalogen precursor” as used herein refers to an ether lipid compound where the sn-1 position is a vinyl ether and the sn-2 position is not an acyl group. Exemplary compounds of plasmalogen precursors are compounds of Formula (I-A), (I-Al), (I- A2), (I-A3), (I-A4), (I-A5), (I-A6). These compounds may be referred to herein as LPC(O), LPE(O) and LPX(O).[000186] As used herein, “acyl alkenyl” refers to a straight or branched chain hydrocarbon containing, for example, from 2 to 30 carbons and containing at least one carbon-carbon double bond, which is covalently bonded to an acyl group. For example, the use of nomenclature such as 22:6 or 18:2 in the context of an acyl alkenyl group refers to an acyl alkenyl group having 22 carbons or 18 carbons respectively, and having 6 or 2 double bonds respectively. An example of an acyl alkenyl group is:[000187] Acyl alkenyl groups may be present in species such as alkylacylglycerols or alkyldiacylglycerols (as an acyl group), or as an acyl group in plasmanyl- or plasmenyl- phospholipids. Typically, when present in those species, there is no double bond between the carbons which are a- and 0- to the acyl group.[000188] As used herein, “acyl alkyl” refers to a straight or branched chain hydrocarbon containing, for example, from 1 to 30 carbons, which is covalently bonded to an acyl group. For example, the use of nomenclature 22:0 or 18:0 in the context of an acyl alkyl group refers to an acyl alkyl group having 22 carbons or 18 carbons respectively. An example of an acyl alkyl group is:[000189] It will also be recognized that the compounds described herein may possess asymmetric centers and are therefore capable of existing in more than one stereoisomeric form. The disclosure thus also relates to compounds that, in at least some embodiments, are in substantially pure isomeric form at one or more asymmetric centers e.g., that have an enantiopurity that is equal to or greater than 90% enantiomeric excess (“ee”), such as 95% ee, 97% ee, 99% ee, or greater than 99% ee. The disclosure also relates to compounds present as mixtures of stereoisomeric forms, including racemic, diastereomeric, or scalemic mixtures. Such isomers may be naturally occurring or may be prepared by asymmetric synthesis, including but not limited to, synthetic methods employing chiral intermediates, or by chiral resolution. Certain compounds contained in the compositions of the present disclosure may exist in particular geometric or stereoisomeric forms. The present disclosure contemplates all such compounds, including cis- and trans-i somers, R- and S-enantiomers, diastereomers, (D)-isomers, (L)-isomers, the racemic mixtures thereof, and other mixtures thereof, as falling within the scope of the disclosure. Additional asymmetric carbon atoms may be present in a substituent such as an alkyl group. All such isomers, as well as mixtures thereof, are intended to be included. If, for instance, a particular enantiomer of a compound of the present disclosure is desired, it may be prepared by asymmetric synthesis, or by derivation with a chiral auxiliary, where the resulting diastereomeric mixture is separated and the auxiliary group cleaved to provide the pure desired enantiomers. Alternatively, where the molecule contains a basic functional group, such as amino, or an acidic functional group, such as carboxyl, diastereomeric salts are formed with an appropriate optically-active acid or base, followed by resolution of the diastereomers thus formed by fractional crystallization or chromatographic means well known in the art, and subsequent recovery of the pure enantiomers.[000190] The present disclosure also relates to derivatives of glycerol. Whilst glycerol is achiral, derivatives are typically chiral. Typically, the glycerol utilized will have a stereochemical configuration corresponding to that found in nature. In some embodiments, the glycerol derivatives utilized have the stereochemical configuration as shown above in Formula (I).[000191] In some embodiments, the plasmalogen precursor compounds described herein are administered or consumed in combination with one or more alkylglycerols. In some embodiments the plasmalogen precursor compounds and alkylglycerols are administered or consumed as separate compositions. In some embodiments plasmalogen precursor compounds and alkylglycerols are combined in a single composition. In some embodiments, the alkylglycerols are derived from natural sources. In some embodiments, the alkylglycerols are synthesized.[000192] As referred to herein, the term “alkylglycerol” means a compound of Formula (I) in which the R1group is a hydrocarbon chain and the R2and R3groups are each hydrogen. The term “alkylglycerol” is additionally taken to mean a compound of Formula (I-A), wherein RA is a hydrocarbon chain, and the Rxgroups are each independently selected from hydrogen or Ci-3alkyl.(I-A)[000193] The term “alkylglycerol” is additionally taken to mean a compound of Formula (I- Al), (I-A2) and (I-A3). Although the term “a / ^y / glycerol” is used, it will be understood by those of skill in the art that the term encompasses species with hydrocarbon groups at the R1position that include unsaturation in the hydrocarbon chain. However, as used herein, an “alkylglycerol” compound does not contain a double bond between carbons 1 and 2 of the hydrocarbon chain, i.e., proximal to the ether linkage.[000194] An alkylglycerol having a “16:0” group is a molecule having an ether bond in the sn-1 position to a 16-carbon saturated hydrocarbon chain, and no double bonds in the chain, which may also be known as chimyl alcohol.[000195] An alkylglycerol having an “18:0” group is a molecule having an ether bond in the sn-1 position to an 18-carbon saturated hydrocarbon chain, and no double bonds in the chain, which may also be known as batyl alcohol.[000196] An alkylglycerol having an “18: 1” group is a molecule having an ether bond in the sn-1 position to an 18-carbon hydrocarbon chain, which contains one double bond, typically between carbons 9 and 10 and typically a c / .s-double bond, which may also be known as selachyl alcohol.[000197] As referred to herein, the term “alkylacylglycerol” means a compound of Formula (I) in which the R1group is a hydrocarbon chain, one of the R2and R3groups is hydrogen, and the other of the R2and R3groups is an acyl group, individual selected from an acyl alkyl group and an acyl alkenyl group. Although the term “a / ^y / acylglycerol” is used, it will be understood by those of skill in the art that the term encompasses species with hydrocarbon groups at the R1position that include unsaturation in the hydrocarbon chain. However, as used herein, an “alkylacylglycerol” does not contain a double bond between carbons 1 and 2 of the R1hydrocarbon chain, i.e., proximal to the ether linkage.[000198] As referred to herein, the term “alkyldiacylglycerol” means a compound of Formula (I) in which the R1group is a hydrocarbon chain, and the R2and R3groups are acyl groups individually selected from acyl alkyl and an acyl alkenyl. Although the term “alkyl acyl glycerol” is used, it will be understood by those of skill in the art that the term encompasses species with hydrocarbon groups at the R1position which include unsaturation in the hydrocarbon chain. However, as used herein, an “alkyldiacylglycerol” does not contain a double bond between carbons 1 and 2 of the R1hydrocarbon chain, i.e., proximal to the ether linkage.[000199] As used herein, the term “LPX(O)” refers to an LPC(O) or an LPE(O) as used elsewhere herein. In some embodiments, the LPX(O) is selected from one or more of LysoPAF-C and LysoPAF-O. In some embodiments, LysoPAF-C is selected from one or more of LysoPAF- C16, LysoPAF-C 18, and LysoPAF-C 18: 1. In some embodiments the LPX(O) is selected from one of more of LPE(O-C16), LPE(O-C18), and LPE(O-C18:1).[000200] The term “fatty acid” may refer to, for example, stearic acid, palmitic acid, or oleic acid.[000201] As used herein, the terms “subject” and “patient” are used interchangeably and refer to individuals to be treated by the methods of the present disclosure. In one embodiment, the subject is a human. In some embodiments, administration may be oral administration, for example, as a liquid, a capsule, a tablet, or a lozenge. In some embodiments, administration may be via any appropriate route including subcutaneous, intravenous, intramuscular, etc.[000202] As used herein, the terms “subject” and “patient” refer to humans or animals to be treated by the methods of the present disclosure. In one embodiment, the subject is a human. In one embodiment, the subject is an animal such as a domestic animal, a working animal or a farm animal. Domestic animals include, but are not limited to, rabbits, birds, cats, dogs, fishes, rats,tortoises, reptiles (lizard, snake) and the like. Working animals include, but are not limited to, cattle, yaks, and horses and the like. Farm animals include, but are not limited to sheep, pigs, cows, chickens, goats, geese, ducks, llamas and the like. In some embodiments, it is envisaged that the compositions described herein will be formulated as an animal feed or dietary supplement for animals. In some embodiments, administration may be oral administration. In some embodiments, administration may be via any appropriate route including a liquid form, a capsule, a tablet, or a lozenge. In some embodiments the appropriate route may be as a high end pet food.[000203] The term “non-disease state” as used herein, refers to a state in which the subject is not suffering from a plasmalogen related disease or deficiency requiring treatment.[000204] As used herein, the term “treating” includes any effect, e.g., lessening, reducing, increasing, maintaining, modulating, ameliorating or eliminating, that results in the improvement of the condition, disease, disorder, and the like, or ameliorating a symptom thereof.[000205] As used herein, the term “effective amount” refers to the amount of a compound (e.g., a compound of the present disclosure) sufficient to effect beneficial or desired results. An effective amount can be administered in one or more administrations, applications or dosages and is not intended to be limited to a particular formulation or administration route.[000206] As used herein, the terms " composition" and “formulation” are used interchangeably and refer to a product comprising a particular ingredient in a particular amount and any product directly or indirectly brought about by the combination of particular ingredients in particular amounts. In some embodiments, a composition comprises an active ingredient and an inactive ingredient. In some embodiments, the composition is a formulation. In some embodiments, the composition or formulation is suitable for administration to and / or consumption by a subject, such as a human. A composition may be a pharmaceutical composition and a formulation may be a pharmaceutical formulation. In some embodiments, the pharmaceutical composition or pharmaceutical formulation comprises a combination of an active agent with a pharmaceutically acceptable carrier, diluent, excipient, solubilizing agent, or vehicle, inert or active. As used herein, the term "pharmaceutically acceptable" means that a carrier, diluent, excipient, solubilizing agent, or vehicle is compatible with other components of a pharmaceutical formulation or pharmaceutical composition and is nontoxic to a subject. Thus, it is to be understood that a “pharmaceutical composition” or a “pharmaceutical formulation” is appropriate for administration to and / or consumption by a subject, such as a human, and may, for example, beapproved by the U.S. Food and Drug Administration and / or the European Medicines Agency for such administration and / or consumption. It is also to be understood that a composition or formulation may not necessarily be, for example, approved by the U.S. Food and Drug Administration and / or the European Medicines Agency for administration to and / or consumption by a subject, such as a human.[000207] Pharmaceutical compositions include a product comprising an active ingredient and an inert ingredient constituting a carrier and include every product directly or indirectly brought about by the combination, complexation or aggregation of any two or more ingredients or the dissociation, other kinds of reactions or interaction of one or more ingredients. Thus, the pharmaceutical composition of the present disclosure includes every composition prepared by mixing the at least one compound of the present disclosure with a pharmaceutically acceptable carrier, diluent, excipient, solubilizing agent, or vehicle.[000208] In some embodiments, a formulation of the disclosure is in the form of a beverage or a food product. In some embodiments, the beverage or food product is formulated for general consumption, such as by being food grade. In some embodiments, the beverage or food product is formulated as a dietary supplement or other nutritional composition. In some embodiments, the beverage or food product is pharmaceutical grade. For the avoidance of doubt, it is to be understood that, in some embodiments, a formulation of the disclosure may be suitable for consumption by a subject, such as a human, but not necessarily be of pharmaceutical grade (for example, by being of food grade or nutritional supplement grade, but not necessarily pharmaceutical grade).[000209] In some embodiments, the formulation may contain one or more of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an anti-foaming agent, or a diluent. The formulation may additionally contain one or more antioxidant compounds. It is anticipated that any antioxidants suitable for oral administration, such as vitamin A, vitamin E, vitamin C, retinal, tocopherol, L-ascorbyl palmitate, riboflavin and carotenoids, including lutein, beta-carotene, zeaxanthin, and lycopene, and combinations thereof, may be formulated into an embodiment described herein. In some embodiments, the composition is naturally unreactive to oxidation and does not require the addition of antioxidant compounds.[000210] As used herein, the term "excipient" shall mean an inactive ingredient used as a vehicle (e.g., water, capsule shell, etc.), a diluent, or a component to constitute a dosage form or composition comprising a drug such as a therapeutic agent. The term also encompasses an inactiveingredient that imparts cohesive function (e.g., binder), disintegrating function (e.g., disintegrator), lubricant function (e.g., lubricating agent), and / or the other function (e.g., solvent, surfactant, etc.) to the composition.[000211] As used herein, the term “pharmaceutically acceptable salt” refers to any pharmaceutically acceptable salt (e.g., acid or base) of a compound of the present disclosure which, upon administration to a subject, is capable of providing a compound of this disclosure or an active metabolite or residue thereof. For example, Berge et al. describe pharmaceutically acceptable salts in detail in J. Pharmaceutical Sciences (1977) 66: 1-19. As is known to those of skill in the art, “salts” of the compounds of the present disclosure may be derived from inorganic or organic acids and bases. The salts can be prepared in situ during the final isolation and purification of the compounds of the disclosure or separately by reacting a free base function with a suitable acid. Examples of acids include, but are not limited to, hydrochloric, hydrobromic, sulfuric, nitric, perchloric, fumaric, maleic, phosphoric, glycolic, lactic, salicylic, succinic, toluene-p-sulfonic, tartaric, acetic, citric, methanesulfonic, ethanesulfonic, formic, benzoic, malonic, naphthalene-2- sulfonic, benzenesulfonic acid, and the like. Other acids while not in themselves pharmaceutically acceptable, may be employed in the preparation of salts useful as intermediates in obtaining the compounds of the disclosure and their pharmaceutically acceptable acid addition salts. Examples of bases include, but are not limited to, alkali metals (e.g., sodium) hydroxides, alkaline earth metals (e.g., magnesium), hydroxides, ammonia, and compounds of formula NW , wherein each W is independently selected from H or Ci-4alkyl, and the like. Basic nitrogen-containing groups can be quatemized with such agents as lower alkyl halides such as methyl, ethyl, propyl, and butyl chlorides, bromides and iodides; dialkyl sulfates like dimethyl, diethyl, dibutyl, and diamyl sulfates; long chain alkyl halides such as decyl, lauryl, myristyl, and stearyl chlorides, bromides, and iodides; arylalkyl halides such as benzyl and phenethyl bromides; and others. Products having modified solubility or dispersibility are thereby obtained.[000212] Examples of salts include, but are not limited to: acetate, adipate, alginate, aspartate, benzoate, benzenesulfonate, bisulfate, butyrate, citrate, camphorate, camphorsulfonate, cyclopentanepropionate, digluconate, dodecyl sulfate, ethanesulfonate, fumarate, flucoheptanoate, glycerophosphate, hemisulfate, heptanoate, hexanoate, hydrochloride, hydrobromide, hydroiodide, 2-hydroxyethanesulfonate, lactate, maleate, methanesulfonate, 2- naphthalenesulfonate, nicotinate, oxalate, palmoate, pectinate, persulfate, phenylpropionate,picrate, pivalate, propionate, succinate, tartrate, thiocyanate, tosylate, undecanoate, and the like. Other examples of salts include anions of the compounds of the present disclosure compounded with a suitable cation such as Na+, NH , and NW (wherein each W is independently selected from H or Ci-4alkyl), and the like. For therapeutic use, salts of the compounds of the present disclosure are contemplated as being pharmaceutically acceptable. However, salts of acids and bases that are non-pharmaceutically acceptable may also find use, for example, in the preparation or purification of a pharmaceutically acceptable compound.[000213] As used herein, the term “carrier” refers to any of the standard carriers, such as a phosphate buffered saline solution, water, emulsions (e.g., such as an oil / water or water / oil emulsions), and various types of wetting agents. In some embodiments, the carrier is of pharmaceutical grade. In some embodiments, the carrier is not of pharmaceutical grade. For example, in some embodiments, the carrier is of food grade, but may not be of pharmaceutical grade. The compositions disclosed herein can also include stabilizers and preservatives. For examples of carriers, stabilizers and adjuvants, see REMINGTON’S PHARMACEUTICAL SCIENCES (Mack Publishing Co., Easton, PA).[000214] The term “day” as used herein is taken to mean a 24 hour period of time.[000215] As a general matter, compositions specifying a percentage are by weight unless otherwise specified.[000216] Ether Lipids and Compositions[000217] The present disclosure shows that ether lipids such as plasmanyl-phospholipids and plasmenyl-phospholipids (plasmalogens) have in vivo profiles which are associated with healthy state, and which are associated with conditions such as diabetes. It has also been found that the in vivo ether lipid profile can be affected by the administration of compositions containing ether lipids to subjects, e.g., by supplementation with krill oil.[000218] The formulations of the present disclosure are useful in maintaining and / or modifying in vivo ether lipid levels at levels and / or ratios associated with a natural, non-disease state (that is, the natural state of a healthy human subject), and / or in modifying or modulating in vivo ether lipid levels towards levels and / or ratios which are associated with a natural, non disease state (that is, the natural state of a healthy human subject). An exemplary, but non-limiting exampleof the term “healthy human subject” is taken to mean a subject or patient who is not suffering from a disease or disorder associated with a plasmalogen deficiency.[000219] Examples of compounds useful in maintaining and / or modifying in vivo ether lipid levels and / or ratios thereof include alkyl glycerols, alkyl acyl glycerols (a compound which is an ether derivable from a glycerol alcohol and an alkyl alcohol, and which has an acyl group derivable from another glycerol alcohol and an acid), alkyl diacyl glycerols, and ether phospholipids, including but not limited to LPC(O)s, LPE(O)s, LPA(O)s, plasmanyl-phospholipids and plasmenyl-phospholipids. In some embodiments, the formulation is for in vivo maintenance and / or in vivo modification of plasmanyl- and / or plasmenyl-phospholipid levels and / or ratios thereof. In some embodiments, the plasmanyl- and / or plasmenyl-phospholipids include those having phosphatidylcholine and / or phosphatidylethanolamine groups. In some embodiments, the formulation is for in vivo maintenance and / or in vivo modification of plasmenyl-phospholipid (plasmalogen) levels and / or ratios thereof. In some embodiments, the formulation is for in vivo maintenance and / or modification of phosphatidylethanolamine plasmenyl-phospholipid (plasmalogen) levels and / or ratios thereof.[000220] Table 2. Examples of plasmanyl-phospholipids, plasmenyl-phospholipids, and related lipidic species, and their abbreviations.Table 2[000221] General reference to “16:0”, “18:0”, and “18: 1” throughout the present disclosure specifies LPX(O)s, covering both LPC(O)s and LPC(O)s, such that “16:0” refers to 16:0 LPX(O), “18:0” refers to 18:0 LPX(O), and “18: 1” refers to 18: 1 LPX(O) as defined herein.[000222] As described herein healthy subjects tend to have a plasmanyl-phospholipid and plasmenyl-phospholipid profile in which certain alkenyl ether and alkyl ether groups are present. For example, a high proportion of ether lipids (e.g., plasmanyl-and / or plasmenyl-phospholipids inclusive of plasmalogens) having 18: 1 alkenyl ether groups, 18:0 alkyl ether groups and 16:0 alkyl ether groups were found in the group of healthy subjects. It is noted that the recited alkyl / alkenyl groups also contain a double bond between carbons 1 and 2 (a cis- vinyl ether group), as described above for several plasmalogen exemplary compounds.[000223] In some embodiments, the formulation is for in vivo maintenance and / or modification of ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) having 18:1 alkenyl ether groups, 18:0 alkyl ether groups and 16:0 alkyl ether groups. In some embodiments, the formulation is for in vivo maintenance and / or modification of levels of plasmalogens having 18: 1ether groups, 18:0 ether groups and 16:0 ether groups. In some embodiments, the formulation is for in vivo maintenance of ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) at, or for in vivo modification of ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) towards, an in vivo total ether lipid (e.g., plasmanyl- and / or plasmenyl-phospholipid) profile in which the ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) have a molar ratio of 18: 1 alkenyl ether groups to 18:0 alkyl ether groups to 16:0 alkyl ether groups of about 1 : 1.7: 1.4. In some embodiments, the formulation is for in vivo maintenance of ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) at, or for in vivo modification of ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) towards, an in vivo total ether lipid (e.g., plasmanyl- and / or plasmenyl- phospholipid) profile in which the ether lipids (e.g., plasmanyl- and / or plasmenyl-phospholipids) have a molar percent of 18: 1 alkenyl ether groups in the range of from 18.6% to 27.9%, a molar percent of 18:0 alkyl ether groups in the range of from 32.6% to 45.8%, and a molar percent of 16:0 alkyl ether groups in the range of from 26.8% to 37.4%; or having a molar percent of 18: 1 alkenyl ether groups of about 23.3%, a molar percent of 18:0 alkyl ether groups of about 39.2%, and a molar percent of 16:0 alkyl ether groups of about 32.1%.[000224] In some embodiments, the formulation is for in vivo maintenance of ether lipids at, or for in vivo modification of ether lipids towards, an in vivo plasmalogen lipid profile in which the ether lipids have a molar ratio of 18: 1 ether groups to 18:0 ether groups to 16:0 ether groups of about 1 : 1.7: 1.4. In some embodiments, the formulation is for in vivo maintenance of ether lipids at, or for in vivo modification of ether lipids towards, an in vivo plasmalogen lipid profile in which the ether lipids have a molar percent of 18: 1 ether groups in the range of from 18.6% to 27.9%, a molar percent of 18:0 ether groups in the range of from 32.6% to 45.8%, and a molar percent of 16:0 ether groups in the range of from 26.8% to 37.4%; or having a molar percent of 18: 1 ether groups of about 23.3%, a molar percent of 18:0 ether groups of about 39.2%, and a molar percent of 16:0 ether groups of about 32.1%.[000225] In some embodiments, the composition comprises at least one isolated compound. In some embodiments, the at least one isolated compound is found at a purity of greater than 99%. In a preferred embodiment, the at least one isolated compound is found at a purity of greater than 99.9%.[000226] In some embodiments the composition comprises a mixture of at least two compounds wherein the % (w / v) of one compound is at least 90%.[000227] Dietary plasmalogens have been studied after krill oil (KO) supplementation in humans, as described in Sung, et al., “Enrichment of n-3 containing ether phospholipids in plasma after 30 days of krill oil compared with fish oil supplementation,” Lipids (2022) 57: 115-124, which is incorporated by reference herein, in its entirety. It has been recognized that ether- containing phospholipids are minor components in plasma and include either alkyl or alkenyl phosphatidylcholine and phosphatidylethanolamine (the latter alkenyl classes being referred to as plasmalogens). It is further noted that while plasmalogen levels are lower than diacyl lipids, even so the plasmalogens are still quite abundant. These have only been studied recently because techniques such as lipidomics have allowed detection and quantitation of these and other minor lipid classes (see, e.g., Meikle, et al., “Postprandial plasma phospholipids in men are influenced by the source of dietary fat,” J. Nutr. (2015) 145(9): 2012-2018). Methods of making certain ether lipids and / or plasmalogen compositions are described in WO 2021 / 007623 Al to Baker Heart and Diabetes Institute, having inventor Meikle, which is incorporated by reference herein in its entirety. There are numerous approaches to the synthesis of these ether lipid compounds using either solely chemical synthesis or a combination of chemical and enzymatic synthesis strategies. Synthesis of AKG compounds have been described in the following papers: Carlos D. Magnusson, et al., “Chemoenzymatic synthesis of a focused library of enantiopure structured l-O-alkyl-2,3- diacyl-sn-glycerol type ether lipids,” Tetrahedron (2011) 67: 1821-1836; and, Arnar Halldorsson, et al., “Lipase catalysed kinetic resolution of 1-O-alkylglycerols by sequential transesterification,” Tetrahedron: Asymmetry (2004) 15: 2893-2899. Similarly, synthesis of the lysoalkenylphosphatidylethanolamine (LPE(P)) from commercially available 2,3-0- isopropylidene-.s / z-glycerol has been described in Guanghui Ni, et al., “Synthesis and evaluation of immunostimulant plasmalogen lysophosphatidylethanolamine and analogues for natural killer T cells,” Bioorg. Med. Chem. (2014) 22(11): 2966-73. Gomes, MAGB, et al. describe the synthesis of numerous alkyl ether lipids (Gomes MAGB, Bauduin A, Le Roux C, Fouinneteau R, Berthe W, Berchel M, Couthon H, Jaffres PA. “Synthesis of ether lipids: natural compounds and analogues,” Beilstein J Org Chem. 2023 Sep 8; 19: 1299-1369). FIG. 2 of Gomes loc cit. discusses a synthetic route that would be adaptable to production of the alkyl LPC(O) compounds of interest, providing the R-groups for the sn-1 fatty acid of interest and stopping at the lyso PAF step. One skilled in the art will appreciate that different protecting groups and / or deprotecting schemes can also be used. FIG. 6 of Gomes and further references disclosed therein describe how to producethe starting compound 1-O-alkylglycerol (i.e., compound 2.1 of FIG. 2 of Gomes). Additionally, U.S. Pat. No. 10,900,063, which is incorporated by reference herein in its entirety, describes the use of lipases to produce LPC(O)s.[000228] LPC(O) Synthetic RoutePG1& PG2are protecting groups, X is leaving group, typically halogenCompound 6, Et3NEt2OStep 6 Step 7 7 8Scheme II. Synthesis of C18.0 LPC(O)[000229] Starting material 1 (R-solketal or R-(-)-2,3-O-isopropylidene-sw-glycerol; CAS 14347-78-5; available from CombiBlocks (98% purity) or Fluorochem (95% purity)) is condensed with either alkyl bromides or mesylates to form corresponding alkyl substituted acetonides (Compound 2). TBAB shown in Scheme II above is tetrabutylammonium bromide, a commonly used phase transfer catalyst. The isopropylidene group can then be removed via acid hydrolysis (Compound 3), and alternative protecting groups applied to arrive at Compound 6. Separately, 2-bromoethyl phosphorodichloridate (Compound 8) is prepared, and then condensed with Compound 6 to give Compound 9. The terminal bromine atom is then replaced by trimethylamine, with a final alcohol deprotection step to afford Compound 11.[000230] As would be readily understood by the skilled person, the reagents and conditions suggested above are merely exemplary and non-limiting. Synthesis of other SN-1 substituted LPC(O)s can be accomplished by, for example, providing appropriate alkyl bromide or alkyl mesylate compounds in step 1. For example, 1 -bromooctadecane (CAS 112-89-0; available from TCI chemicals, >97.0% purity as determined by gas chromatography); oleyl mesylate (prepared by mesylation of oleyl alcohol: CAS 143-28-2; available from Sigma Aldrich, 85% purity as determined by gas chromatography); and 1 -bromohexadecane (CAS 112-82-3; available from TCI chemicals, 96% purity as determined by gas chromatography) can be used in the synthesis of C18:0, C18: l and Cl 6:0 LCP(O)s respectively.[000231] Suitable protecting groups for alcohol moieties are well known in the art (see, for example, Greene's Protective Groups in Organic Synthesis, Wiley, DOI: 10.1002 / 9781118905074).[000232] LPE(O) Synthetic Route[000233] Synthesis of the corresponding LPE(O) compounds can be carried out in a similar manner using substituted ammonium compounds instead of trimethylamine in step 8. The ammonium compound can then be deprotected to leave an NELC group. Such deprotection may take place alongside the alcohol deprotection in step 9, or via an additional synthetic step, depending on the nature of the substituents and protecting groups chosen. Alternative exemplary and non-limiting syntheses include:(i) saturation of the vinyl double bond of LPE(P) alkenyl compounds produced by the method of Ni et al. loc cit, with chemical (typically nickel) or enzymatic reduction, which provides an alternative synthesis of LPE(O)s; and(ii) hydrolysis of the SN2 group of commercially available alkyl PE compounds, such as l-hexadecyl-2-(9Z-octadecenoyl)-sn-glycero-3-phosphoethanolamine (Cat 878130) from e.g. Avanti Polar Lipids (<avantilipids.com>), using chemical or enzymatic means, such as an appropriate lipase to give C16.0 alkyl LPE(O).[000234] In a particular embodiment, a combination of lysoakylphosphatidylcholine (LPC(O)), or lysoalkylphosphatidylethanolamine (LPE(O)) compounds is contemplated. Derivatives of the aforementioned compounds are contemplated. One exemplary embodiment comprises a specific formulation of three species of lysoalkylphosphatidylcholine (LPC(O)). The species may include LPC(O-18: 1), shown as compound (I-Al) below, LPC(O-18:0), compound (I-A2), and LPC(O-16:0), compound (I-A3). These ether lipids may have a molar ratio of R1groups of about 1.0: 1.7: 1.4, for example. The ratios may be varied among different cellular target populations and different subjects.[000235] In this preferred embodiment, the compounds are depicted as follows, as LPC(O- 18: 1):(I-A3)[000238] Other compounds and combinations are also contemplated, such as a combination of lysoalkylphosphatidylethanolamines (LPE(O)), including LPE(O-18: 1), shown as compound (I-A4) below, LPE(O-18:0), compound (I-A5), and LPE(O-16:0), compound (I-A6). Molar ratios of R1groups may be varied, as well as molar percentages and weight percentages.[000239] In this embodiment, the compounds are depicted as follows, as LPE(O-18: 1):(I-A6)[000242] Other compounds and combinations are also contemplated, such as a combination of lysoalkylphosphatidic acids (LPA(O)), which are phosphate compounds, including LPA(O- 18: 1), shown as compound (I-A7) below, LPA(O-18:0), compound (I-A8), and LPA(O-16:0), compound (I-A9). Molar ratios of R1groups may be varied, as well as molar percentages and weight percentages.[000243] In this embodiment, the compounds are depicted as follows, as LPA(O-18: 1):(I-A7)[000244] LPA(O-18:0):(I-A9)[000246] When ingested, these phosphocholine species, in particular the LPC(O)s, are absorbed in the intestine and then metabolized into a series of ether phospholipids that include: alkyphosphatidylcholine (PC(O)), alkylphosphatidylethanolamine (PE(O)), alkenylphosphatidylcholine (plasmalogen, PC(P)) and alkenylphosphatidylethanolamine (plasmalogen, PE(P)). In studies, this led to increased levels of both the PC(P) and PE(P) species, which are bioactive species with a number of desirable health properties. The bioavailability and conversion of the LPC(O) into PC(P) and PE(P) is 5-12-fold higher than the commonly used alkylglycerol (AKG) species also used to increase plasmalogen levels. Without wishing to be bound by theory, it is believed that this means that lower doses can be used to achieve the same elevation of plasmalogens.[000247] In some embodiments, the compounds are not marine-sourced (i.e., the compounds are not obtained from marine sources). In some embodiments, the compounds are not obtained from shark liver oil. In some embodiments, the compounds are not obtained from fish oil. In some embodiments, the compounds are not obtained from krill. In some embodiments, the compounds are synthesized. Exemplary methods of synthesis are disclosed herein.[000248] In some embodiments, the compositions may be in any product form comprising the ingredients described herein, and which is safe and effective for oral administration.[000249] A further embodiment contemplated by the present disclosure is a formulation, which may be in the form of a food, such as a dietary supplement, that, upon ingestion leads to an increased level of plasmalogens within the blood and tissues of the recipient and thereby ameliorates or overcomes any plasmalogen deficiency that may exist within said individual. Increasing the levels of plasmalogens may lead to improved health outcomes. Such a formulation, for example, an LPC(O) formulation, could also be incorporated into a range of foods to facilitate delivery to the recipient. The intended recipients would be anyone who is deficient in plasmalogens and / or who is at risk of any of a range of metabolic diseases where plasmalogens may play a protective role.[000250] As used herein, the term “dietary supplement” refers to a food product intended to enhance the diet of the subject and thereby improve nutrition. Dietary supplements may include the compositions described herein alone, or alongside other ingredients intended to supplement the diet, such as vitamins and minerals, fibre, herbs and other botanical extracts including flower remedies, homeopathic remedies, amino acids, enzymes and live microbials, probiotics, prebiotics or any combination thereof. Dietary supplements may be formulated in a wide variety of ways including as oils, gummies, drops, capsules, rapid-melt formulations, lozenges, oral sprays, chewing gums, gels, powders, premixed drinks, meal replacement shakes, or bars.[000251] An example of a foodstuff into which a formulation as described herein can be incorporated, is infant formula. Foods in which a formulation comprising, for example, LPC(O)s can be incorporated include infant formula, follow-on formula, Medical Foods and Foods for Special Medical Purposes.[000252] An example of a foodstuff into which a composition or formulation as described herein can be incorporated is any food stuff formulated for human consumption.[000253] The terms “Medical Foods” or “Foods for Special Medical Purposes” as used herein refer to foodstuffs that are specially formulated and intended for the dietary management of a disease, disorder or condition that has distinctive nutritional needs that cannot be met by normal diet alone. Medical Foods assist patients who are temporarily or permanently unable to achieve an adequate nutritional intake from normal foods or through modification of the normal diet and are either malnourished or at risk of becoming malnourished. Medical Foods are used under medical supervision and may be administered orally or via tube feeds (e.g., nasogastric tubes). These terms as used herein are referred to under Regulation (EU) No 609 / 2013 and (Foodand Drug Authority (FDA)) 21 CFR 101 ,9(j)(8)(ii). They are thus distinguished from dietary supplements which are generally available for consumption without medical supervision. [000254] The term “infant” as used herein, is taken to mean a person aged 12 months or younger. The term “infant” is taken to additionally mean “pre-term infant”, which is a person aged 12 months or younger, who was bom prior to 36 weeks of gestation. The term “toddler” as used herein, is taken to mean a person greater than one year of age up to three years of age. The term “child” or “children” as used herein, refers to a person greater than three years of age, up to 12 years of age. The terms “infant formula” as used herein, unless otherwise specified, refers to liquid, semi-liquid, solid and semi-solid human milk replacements or substitutes that are suitable for consumption by an infant. The synthetic formulas include components that are of semipurified or purified origin. As used herein, the terms “semi-purified” and “purified” refer to a material that has been prepared by purification of a natural material or by synthesis. The term “infant formula” is not taken to include unmodified human breast milk.[000255] The infant formula may include liquid and powdered dietary supplements, liquid and powdered human milk fortifiers, liquid and powdered preterm infant formulas, liquid and powdered infant formulas, liquid and powdered elemental and semi-elemental formulas, liquid and powdered toddler formulas, and powdered follow - on formulas suitable for use infants and children. Compositions may be in any product form comprising the ingredients described herein, and which is safe and effective for oral administration.[000256] The infant formula may further include ingredients including, protein, fat, carbohydrate, vitamins, minerals, anti-caking agents, and emulsifiers. In some embodiments, the formula may contain purified cow's milk whey and / or casein as a protein source, a blend of vegetable oils as a fat source, lactose as a carbohydrate source, a vitamin-mineral mix, and other ingredients including, but not limited to, any antioxidants suitable for oral administration such as vitamin A, vitamin E, vitamin C, retinal, tocopherol, L-ascorbyl palmitate, riboflavin and carotenoids, including lutein, beta-carotene, zeaxanthin, and lycopene, and combinations thereof. The infant formula may include oils, for example, vegetable oil including, for example, high oleic sunflower oil, coconut oil, canola oil, sunflower oil, or fish oil, and combinations thereof. The infant formula may include milk products and derivatives from milk, including, for example, lactose, milk proteins, galacto-oligosaccharides, whey concentrate, fructo-oligosaccharides,further compounds enriched from milk(s) secreted by mammals including, but not limited to human, bovine, etc..[000257] The infant formula may include anti-caking agents such as tricalcium phosphate, potassium chloride, sodium citrate, and potassium citrate, magnesium hydrogen phosphate, and coagulants, such as for example magnesium chloride, choline chloride, L-ascorbic acid, emulsifier iron (II) sulfate, zinc sulfate.[000258] The powders may be reconstituted with water prior to use to a caloric density tailored to the nutritional needs of the ultimate user, although in most instances the powders are reconstituted with water to form compositions comprising at least 19 kcal / fl oz (660 kcal / liter), more typically from about 20 kcal / fl oz (675-680 kcal / liter) to about 25 kcal / fl oz (820 kcal / liter), even more typically from about 20 kcal / fl oz (675-680 kcal / liter) to about 24 kcal / fl oz (800-810 kcal / liter). Generally, the 22-24 kcal / fl oz formulas are more commonly used in preterm or low birth weight infants, and the 20-21 kcal / fl oz (675-680 to 700 kcal / liter) formulas are more often used in term infants. In some embodiments, the reconstituted powder may have a caloric density of from about 50-100 kcal / liter to about 660 kcal / liter, including from about 150 kcal / liter to about 500 kcal / liter. In some specific embodiments, the emulsion may have a caloric density of 25, or 50, or 75, or 100 kcal / liter.[000259] When the nutritional product is a powdered infant formula, the protein component is present in an amount of from about 5% to about 35%, including from about 8% to about 12%, and including from about 10% to about 12% by weight of the infant formula; the fat component is present in an amount of from about 10% to about 35%, including from about 25% to about 30%, and including from about 26% to about 28% by weight of the infant formula; and the carbohydrate component is present in an amount of from about 30% to about 85%, including from about 45% to about 60%, including from about 50% to about 55% by weight of the infant formula.[000260] The infant formulas contemplated herein may be formulated to include at least one of fat, protein, and carbohydrate, and preferably also contains vitamins, minerals, and at least one compound of Formula (I), (I-A), (I-Al), (I-A2), (I-A3), (I-A4), (I-A5), and / or (I-A6) or combinations thereof.[000261] The formulas may also be contemplated for use in adult populations in addition to a normal diet or as meal replacement therapy. Nutritional products, medical foods, foods forspecial medical purposes, or dietary supplements may be formulated as meal replacements or supplements for adults. Meal replacement therapy is especially useful for adults with advanced neurological diseases such as Alzheimer’s and Parkinson’s as they may have issues chewing and swallowing and postpartum patients to support healthy breast milk production.[000262] The term “Meal replacement therapy” refers to foods generally eaten at a set time, such as standard meal times (e.g. breakfast, lunch, dinner), being replaced by foods which are formulated to provide a balanced and healthy mixture of macronutrients. These may contain carbohydrates, fat and protein, as well as fibre, vitamins and minerals. These may be in the form of a shake or liquid which is orally ingested.[000263] There are many disease settings where plasmalogens have been demonstrated to play a protective role. These include, but are not limited to: metabolic disorders (obesity, insulin resistance, type 2 diabetes; nonalcoholic fatty liver disease, nonalcoholic steatohepatitis); immune related diseases (asthma, atopic dermatitis, type 1 diabetes, infection); cardiovascular disease (atherosclerosis, cardiac remodeling, hypertension); neurological diseases (Alzheimer’s disease; Parkinson’s disease, autism, amyotrophic lateral sclerosis, frontotemporal dementia; multiple sclerosis; schizophrenia); cancer; myalgic encephalomyelitis / chronic fatigue syndrome; Barth syndrome; peroxisomal disorders (Zellweger syndrome spectrum disorders, rhizomelic chondrodysplasia punctata). These have been reviewed in several recent papers, as follows: Tremblay, et al., “Plasmalogens and platelet-activating factor roles in chronic inflammatory diseases,” BioFactors (2022) 1-14; Schooneveldt, et al., “Ether lipids in obesity: from cells to population studies,” Frontiers in Physiology (March 2022) 13: 1-11; Boselli, Jr., et al., “Plasmalogen replacement therapy,” Membranes (2021) 11 : 838; and, S. Paul, G.I. Lancaster, and P. Meikle, “Plasmalogens: a potential therapeutic target for neurodegenerative and cardiometabolic disease,” Progress Lipid Res. (2019) 74: 186-195.[000264] The formulations of the disclosure are based on the proportional levels of the corresponding PE(P) species in circulation or tissues, and accordingly, specific formulations may be used to target specific fluids e.g., plasma), tissues, such as liver, heart, or fat tissues, or specific cell types, such as immune cells. With regard to targeting plasma, an embodiment of a contemplated formulation comprises ether lipids having a molar ratio of 18: 1 alkenyl / alkyl R1groups to 18:0 alkyl R1groups to 16:0 alkyl R1groups of about 1.0: 1.7: 1.4, having a molar percent of 18: 1 ether groups in the range of from 18.6% to 27.9%, having a molar percent of 18:0 ethergroups in the range of from 32.6% to 45.8%, or having a molar percent of 16:0 ether groups in the range of from 26.8% to 37.4%.[000265] With regard to targeting immune cells, an embodiment of a contemplated formulation comprises ether lipids having a molar ratio of 18:1 alkenyl / alkyl R1groups to 18:0 alkyl R1groups to 16:0 alkyl R1groups is about 1.0:3.4:3.3.[000266] An embodiment of a contemplated formulation or composition comprises at least one compound of Formula (I). In certain embodiments, the at least one compound of Formula (I) is a compound of Formula (I-A). In certain embodiments, the at least one compound of Formula (I-A) is one or more of Formula (I-Al), Formula (I-A2) and / or Formula (I-A3). In certain embodiments, the at least one compound of Formula (I) is a mixture of two compounds of Formula (I). In certain embodiments, the at least one compound of Formula (I) is a mixture of two compounds of Formula (I-A). In certain embodiments, the at least one compound of Formula (I- A) is a mixture of two compounds selected from Formula (I-Al), Formula (I-A2) and Formula (I- A3). In certain embodiments, the at least one compound of Formula (I-A) is a mixture of Formula (I-Al), Formula (I-A2) and Formula (I-A3).[000267] In certain embodiments, the mixture of Formula (I-Al), Formula (I-A2) and Formula (I-A3) makes up at least 50% of the ether lipids in the on a molar percentage basis. In certain embodiments, the mixture has a molar ratio of from 1.2:1 to 2.5:1 of (I-A2) to (I-Al). In certain embodiments, the mixture has a molar ratio of from 1.5:1 to 2.1:1 of (I-A2) to (I-Al). In certain embodiments, the mixture has a molar ratio of 1.7:1 of (I-A2) to (I-Al). In certain embodiments, the mixture has a molar ratio of from 0.9:1 to 1.7:1 of (I-A2) to (I-A3). In certain embodiments, the mixture has a molar ratio of from 1:1 to 1.5:1 of (I-A2) to (I- A3). In certain embodiments, the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I- A3). In certain embodiments, the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I-A3). In certain embodiments, the mixture has a molar ratio of from 0.6:1 to 0.9:1 of (I-Al) to (I-A3). In certain embodiments, the mixture has a molar ratio of 0.72: 1 of (I-Al) to (I-A3). In certain embodiments, the mixture has a molar percent of (I-Al) of from 18.6% to 27.9%, of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%. In certain embodiments, the mixture has a molar percent of (I-Al) of 23.3%, a molar percent of (I-A2) of 39.2%, and a molar percent of (I-A3) of 32.1%. In certain embodiments, the mixture has a molar ratio of (I-A1):(I-A2):(I-A3) of 1:1.7: 1.4.[000268] In certain embodiments, the at least one compound of Formula (I), (I-A), (I-Al), (I-A2) and / or (I-A3) is converted to at least one plasmalogen in vivo.[000269] An embodiment of a contemplated formulation or composition as disclosed herein comprises at least one compound of Formula (I). In certain embodiments, the at least one compound of Formula (I) is a compound of Formula (I-A). In certain embodiments, the at least one compound of Formula (I-A) is one or more of Formula (I-A4), Formula (I-A5) and / or Formula (I-A6) In certain embodiments, the at least one compound of Formula (I) is a mixture of two compounds of Formula (I). In certain embodiments, the at least one compound of Formula (I) is a mixture of two compounds of Formula (I-A). In certain embodiments, the at least one compound of Formula (I-A) is a mixture of two compounds selected from Formula (I-A4), Formula (I-A5) and Formula (I-A6). In certain embodiments, the at least one compound of Formula (I-A) is a mixture of Formula (I-A4), Formula (I-A5) and Formula (I-A6).[000270] In certain embodiments, the mixture of Formula (I-A4), Formula (I-A5) and Formula (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis. In certain embodiments, the mixture has a molar ratio of from 1.2:1 to 2.5 : 1 of (I-A5) to (I- A4). In certain embodiments, the mixture has a molar ratio of from 1.5:1 to 2.1:1 of (I-A5) to (I- A4). In certain embodiments, the mixture has a molar ratio of 1.7:1 of (I-A5) to (I-A4). In certain embodiments, the mixture has a molar ratio of from 0.9:1 to 1.7:1 of (I-A5) to (I-A6). In certain embodiments, the mixture has a molar ratio of from 1:1 to 1.5:1 of (I-A5) to (I-A6). In certain embodiments, the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6). In certain embodiments, the mixture has a molar ratio of from 0.5:1 to 1:1 of (I-A4) to (I-A6). In certain embodiments, the mixture has a molar ratio of from 0.6:1 to 0.9:1 of (I-A4) to (I-A6). In certain embodiments, the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6). In certain embodiments, the mixture has a molar percent of (I-A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 2.8% to 37.4%. In certain embodiments, the mixture has a molar percent of (I-A4) of 24.8%, a molar percent of (I-A5) of 42.4%, and a molar percent of (I-A6) of 32.8%. In certain embodiments, the mixture has a molar ratio of (I-A4):(I-A5):(I-A6) of 1:1.7: 1.4.[000271] In certain embodiments, the at least one compound of Formula (I), (I-A), (I-A4), (I-A5) and / or (I-A6) is converted to at least one plasmalogen in vivo.[000272] In certain embodiments, the mixture of the at least one compound of Formula (I) or (I-A), is a mixture of compounds of (I-Al), (I-A2), (I-A3), (I-A4), (I-A5) and / or (I-A6).[000273] It is expected that the above-disclosed ratios of the above formulations will produce therapeutically effective ratios of plasmalogens PE(P) and PC(P) in the serum and tissues of a human subject who is administered or consumes the formulations.[000274] Other useful phosphatidyl classes can be prepared in accordance with the principles herein, for examples phosphatidyl serines, and phosphatidyl inositols.[000275] In further embodiments, the LPC(O)s, LPE(O)s, and LPA(O)s may be used in various advantageous combinations which may be effective to increase plasmalogen levels. The plasmalogens which are potentiated or modulated are generally represented by those listed above. [000276] In certain embodiments, the above-described formulations include one or more liquid or gel-based carriers, including, but not limited to, those selected from the group consisting of water and physiological salt solutions, urea, alcohols and derivatives thereof (e.g., methanol, ethanol, propanol, butanol), glycols (e.g., ethylene glycol, propylene glycol), and the like; natural or synthetic flavorings and coloring agents; thickening agents, including, but not limited to, those selected from the group consisting of com starch, guar gum, xanthan gum, and the like. In certain embodiments, the one or more liquid or gel-based carrier(s) can be added to the formulations in a weight / volume percentage of from about 0.5% to about 95% weight / volume of the formulation. In certain embodiments, the natural or synthetic flavoring(s) can be added to the formulations in a weight / volume percentage of from about 3.0% to about 10.0% weight / volume of the formulation. In certain embodiments, the coloring agent(s) can be added to the formulations in a weight / volume percentage of from about 1.0% to about 10.0% weight / volume of the formulation. In certain embodiments, the thickening agent(s) can be added to the formulations in a weight / volume percentage of about 2% weight / volume of the formulation.[000277] Delivery System[000278] The formulations disclosed herein may be delivered via dosage forms including, but not limited to, tablets, capsules, solutions, suspensions, powders, gums, and confectionaries. The formulations disclosed herein may be delivered via sublingual delivery systems including, but not limited to, dissolvable tabs under and on the tongue, liquid drops, and beverages. Alternatively, or in addition, edible films, hydrophilic polymers, oral dissolvable films, or oral dissolvable strips can be used.[000279] For oral administration, the formulations disclosed herein may be further combined with one or more solid inactive ingredients for the preparation of tablets, capsules, pills, powders, granules, or other suitable dosage forms. For example, the formulation components may be combined with at least one excipient including, but not limited to, those selected from the group consisting of fillers, binders, humectants, disintegrating agents, solution retarders, absorption accelerators, wetting agents, absorbents, and lubricating agents. Other useful excipients include, but are not limited to, magnesium stearate, calcium stearate, mannitol, xylitol, sweeteners, starch, carboxymethylcellulose, microcrystalline cellulose, silica, gelatin, silicon dioxide, and the like. In some embodiments, formulations according to the disclosure may include one or more of beeswax (such as beeswax E901), carnauba wax (such as carnauba wax E903), shellac (such as shellac E904), candelilla wax (such as candelilla wax E902), microcrystalline wax (such as microcrystalline wax E905), paraffin wax, and di-acylglycerols.[000280] The components of the formulations administered according to the methods of the present disclosure can be administered in a wide variety of oral dosage forms. It will be obvious to those skilled in the art that suitable dosage forms may comprise, in certain embodiments one or more chemical compounds of the present disclosure and / or one or more acceptable salts of a chemical compound of the present disclosure.[000281] For preparing formulations or compositions to be administered according to the methods of the present disclosure, acceptable carriers can be either solid or liquid. Solid form preparations include powders, tablets, pills, capsules, and cachets. A solid carrier can be one or more substances that may also act as diluents, flavoring agents, solubilizing agents, lubricants, suspending agents, binders, preservatives, tablet disintegrating agents, or encapsulating materials. [000282] In powders, the carrier is a finely divided solid, which is in a mixture with the finely divided active component. In tablets, one or more compounds of the present disclosure and / or acceptable salts thereof is mixed with one or more carriers having the necessary binding capacity in suitable proportions, which is then compacted in the shape and size desired.[000283] In certain embodiments, powders and tablets administered according to methods of the present disclosure preferably may contain, in total, from about one to about ninety-nine percent, such as from five or ten to about seventy percent one or more compounds of the present disclosure and / or acceptable salts thereof. Suitable carriers include, but are not limited to, are magnesium carbonate, magnesium stearate, talc, sugar, lactose, pectin, dextrin, starch, gelatin, tragacanth,methylcellulose, sodium carboxymethylcellulose, a low melting wax, cocoa butter, and the like. The term “preparation” is intended to include the formulation of one or more compounds of the present disclosure and / or acceptable salts thereof with encapsulating material as a carrier providing a capsule in which one or more compounds of the present disclosure and / or acceptable salts thereof, with or without additional carriers, is surrounded by a carrier, which is thus in association with it. Similarly, cachets and lozenges are included. Tablets, powders, capsules, pills, cachets, and lozenges are included. Tablets, powders, capsules, pills, cachets, lozenges and rapid melts can be used as solid forms suitable for oral administration.[000284] Capsules may be prepared in such a way as to be additionally coated for timed release. Coating thickness may be modified to provide a delayed release of the capsule contents. Capsules may be prepared in such a way as to be targeted release capsules. In some embodiments, the capsule can be targeted to the stomach. In some embodiments, the capsule targeted for delivery to the stomach is coated in a film coating. In some embodiments, the capsule can be targeted to the small intestine. In some embodiments, the capsule targeted for delivery to the small intestine is coated in an enteric coating.[000285] The term “rapid-melt” as used herein refers to formulations that melt on contact with saliva requiring little or no chewing.[000286] Liquid preparations include, but are not limited to, solutions, suspensions, and emulsions, for example, water or water-propylene glycol solutions. The formulated preparations may take such forms as suspensions, solutions, or emulsions in oily or aqueous vehicles, and may contain formulation agents such as suspending, stabilizing, solubilizing, and / or dispersing agents. Alternatively, one or more compounds of the present disclosure and / or acceptable salts thereof may be in powder form, such as that obtained by aseptic isolation of sterile solid or by lyophilization from solution, for constitution with a suitable vehicle, e.g., sterile, pyrogen-free water, before use.[000287] Aqueous solutions suitable for oral use can be prepared by dissolving one or more compounds of the present disclosure, and / or acceptable salts thereof, in water, and adding suitable colorants, flavors, stabilizing and thickening agents, as desired. Aqueous suspensions suitable for oral use can be made by solubilizing, and / or dispersing the finely divided active component in water with viscous material, such as natural or synthetic gums, resins, methylcellulose, sodium carboxymethylcellulose, or other well-known suspending agents.[000288] Formulations suitable for topical administration in the mouth, or buccal, or sublingual administration include, but are not limited to: lozenges comprising the active agent in a flavored base, usually sucrose and acacia or tragacanth; pastilles comprising the active ingredient in an inert base such as gelatin and glycerine or sucrose and acacia; and mouthwashes comprising the active ingredient in suitable liquid carrier.[000289] In some embodiments, a formulation comprises a solubilizing agent. As used herein, the term “solubilizing agent” refers to any agent which promotes solubilization or dispersal of the composition when placed into a liquid. In some embodiments, a “solubilizing agent” may be a dispersal agent. The solubilizing agent may additionally improve the stability of the formulated composition. Suitable solubilizing agents include, but are not limited to, carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, solvents, phospholipids, such as lecithin (including, but not limited to, egg yolk L-a-lecithin, such as egg yolk L-a-lecithin available from Sigma-Aldrich, Saint Louis, M.O., U.S.A.), DMSO, ethanol, ethyl acetate, isopropanol, and the like. In some embodiments, a solubilizing agent is used to improve the separation of the compounds which make up the formulation and to prevent their settling or clumping in formulations. In some embodiments, a formulation comprises a solubilizing agent and a suitable carrier. In some embodiments, such a formulation is a pharmaceutical -grade product. In some embodiments, such a formulation is a food-grade product.[000290] The formulations or preparations are preferably in unit dosage forms. In such form, the formulation is subdivided into unit doses containing appropriate quantities of the active component. The unit dosage form can be a packaged preparation, the package containing discrete quantities of preparation, such as packaged tablets, capsules, and powders in vials or ampoules. Also, the unit dosage form can be a capsule, tablet, cachet, or lozenge itself; or it can be the appropriate number of any of these in packaged form.[000291] Tablets, capsules, and lozenges for oral administration and liquids for oral use are preferred formulations.[000292] Further details on techniques for formulation and administration may be found in the latest edition of REMINGTON’ S PHARMACEUTICAL SCIENCES (Mack Publishing Co., Easton, PA).[000293] Routes of Administration and Dosages[000294] The compounds of the present disclosure and / or acceptable salts thereof may be administered by any route, including, but not limited to, oral, sublingual, buccal, or as an oral spray.[000295] Given the improved bioavailability of LPC(O)s various combinations of LPC(O)s, LPE(O)s, and LPA(O)s are contemplated for use in the formulations. Dosages may be varied as appropriate to age, height, and weight of the subject. Doses and dosage amounts are referred to below as LPX(O) equivalents. LPX(O) equivalent is taken to mean that any LPC(O), LPE(O) or LPA(O) compound either alone or in combination with any other LPX(O) compounds is provided as a dose in the amount specified.[000296] In some embodiments, a useful human dose is 2-3 mg / kg, amounting to 100-300 mg, LPX(O) equivalents per subject per day. In a particular embodiment, a useful dose is 200 mg LPX(O) equivalents per subject per day.[000297] In some embodiments, the dose may be 0.2-2 mg / kg, 25-100 mg LPX(O) equivalents per subject per day. That is, for some subjects, the dose may be 25 mg, 50 mg, or 100 mg LPX(O) equivalents per subject per day.[000298] In some embodiments, a dose may be 50 mg to 2 g LPX(O) equivalents per subject per day. In some embodiments, a dose may be 50 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 100 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 150 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 200 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 250 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 300 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 350 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 400 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 450 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 500 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 550 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 600 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 650 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 700 mg LPX(O) equivalents per subject per day. In someembodiments, a dose may be 750 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 800 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 850 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 900 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 950 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1000 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1050 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1100 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1150 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1200 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1250 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1300 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1350 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1400 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1450 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1500 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1550 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1600 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1650 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1700 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1750 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1800 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1850 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1900 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 1950 mg LPX(O) equivalents per subject per day. In some embodiments, a dose may be 2000 mg LPX(O) equivalents per subject per day.[000299] In some embodiments, for example if a large elevation of plasmalogens is desirable or a rapid elevation thereof, a dose may be 3-25 mg / kg, 300-2000 mg LPX(O) equivalents per subject per day. That is, a suitable dose may be 400 mg, 800 mg, or 1600 mg LPX(O) equivalents per subject per day.[000300] In some embodiments, a dose may be 25-50 mg / kg, 2000-4000 mg LPX(O) equivalents per subject per day. That is, a suitable dose may be 2000 mg, 2500 mg, 3000 mg, 3500 mg, or 4000 mg LPX(O) equivalents per subject per day.[000301] In some embodiments, a dose may be 2-337 mg / kg, 1.6-78 g LPX(O) equivalents per subject per day. In some embodiments, an acute dose may be 150-337 mg / kg, 12-27 g LPX(O) equivalents per subject per day. In some embodiments, a prophylactic dose may be 2- 130 mg / kg, 1.6-78 g LPX(O) equivalents per day.[000302] In some embodiments, a dose of LPX(O) may be 0.2-1.5% by weight of a subject’s total diet per day. In some embodiments, an acute dose of LPX(O) may be 1.5% by weight of a subject’s total diet. In some embodiments, a prophylactic dose may be 0.02-0.75% by weight of a subject’s total diet.[000303] In some embodiments, a dose may be 0.1-4000 mg LPX(O) equivalents per subject per day.[000304] In some embodiments, a dose may be 30 mg, 100 mg, or 300 mg LPX(O) equivalents per subject per day.[000305] In some embodiments the infant formula or meal replacement therapy may include a dose of 0.1 - 200 mg / L LPX(O) equivalents. In some embodiments the infant formula or meal replacement therapy may include a dose of 10 - 100 mg / L LPX(O) equivalents. In some embodiments the infant formula or meal replacement therapy may include a dose of 25 - 100 mg / L LPX(O) equivalents. In some embodiments the infant formula or meal replacement therapy may include a dose of about 64 mg / L LPX(O) equivalents.[000306] In some embodiments the pet food may include a dose of 0.1 - 200 mg / L LPX(O) equivalents. In some embodiments, a dose may be 0.1-4000 mg LPX(O) equivalents.[000307] In some embodiments, one or more poly or monounsaturated fatty acids may be added to the LPX(O) composition to further increase plasmalogens and / or support infant nutrition, improve heart and metabolic health, improve and / or treat neurodevelopment and brain health, alleviate liver damage, and to treat inflammation. In some embodiments, the fatty acid is an omega 3 fatty acid such as DHA, ALA (alpha-linolenic acid), or EPA (Eicosapentaenoic acid). In some embodiments, the dose of omega 3 fatty acids is 2-5 g / day. In some embodiments, the dose of omega 3 fatty acids is 250-500 mg / day. In some embodiments the ratio of DELAEPA is 1 :2, 1 : 1, or 2: 1. In some embodiments, the DELAEPA ratio is> 2: 1. In some embodiments thefatty acid is an omega 6 fatty acid such as ARA, which has been shown to be very important for brain development and cognitive decline (J Adv Res. 2017 Nov 24; 11 :33-41. doi: 10.1016 / j.jare.2017.11.004). In some embodiments, 100 mg / day of DHA and 140 mg / day ARA are recommended for infant nutrition. In some embodiments, at least about 0.2-0.4% of formula is DHA and at least about 0.35-0.7% of infant formula ARA.[000308] The use of any and all examples, or exemplary language (e.g., “such as”) provided herein, is intended merely to better illuminate the disclosure and does not pose a limitation on the scope of the disclosure unless otherwise stated. No language in the specification should be construed as indicating any non-claimed element as essential to the practice of the disclosure.[000309] The methods described above may be further understood in connection with the following Examples. In addition, the following non-limiting examples are provided to illustrate the disclosure. However, the person skilled in the art will appreciate that it may be necessary to vary the procedures for any given embodiment of the disclosure, e.g., vary the order or steps.[000310] While in the foregoing specification this disclosure has been described in relation to certain embodiments thereof, and many details have been put forth for the purpose of illustration, it will be apparent to those skilled in the art that the disclosure is susceptible to additional embodiments and that certain of the details described herein can be varied considerably without departing from the basic principles of the disclosure.[000311] All references cited herein are incorporated by reference in their entireties. The present disclosure may be embodied in other specific forms without departing from the spirit or essential attributes thereof, and, accordingly, reference should be made to the appended claims, rather than to the foregoing specification, as indicating the scope of the disclosure.[000312] In some embodiments, the composition is a meal replacement therapy.[000313] In some embodiments, the meal replacement therapy is formulated for an adult subject.[000314] In some embodiments, the meal replacement therapy is formulated for an infant subject.[000315] In some embodiments, the treatment further comprises the use or administration of one or more alkylglycerols, PE(O), PC(O), and / or DHA compounds.[000316] In some embodiments, a method is provided for increasing the levels of PE(O)s and / or PC(O)s in a subject comprising administering one or more compounds as defined hereinto the subject, including PE(O)s and / or PC(O)s. The beneficial effects of PE(O)s and / or PC(O)s is exemplified at least in Example 10 for plasmalogen-associated disorders, such as metabolic disorders, obesity and liver disorders. Beneficial effects of PE(O)s and / or PC(O)s are further exemplified at least in Figures 35-43 and Example 22.[000317] The present disclosure further demonstrates that LPX(O)s increases PX(O) levels, at least in Figures 20B and 20B, Figures 19A and 19B, and Figure 63 with respect to serum levels, Figure 65 with respect to liver levels, Figure 88 with respect to heart tissue, and throughout Example 21 for neuronal levels, further exemplified by Figure 96. Accordingly, the present disclosure establishes a link between LPX(O) administration and PX(O) levels.[000318] Plasmalogen-associated disorders[000319] In some embodiments, the composition of the present disclosure is beneficial in the treatment of plasmalogen-associated disorders. In some embodiments, the composition is provided for the treatment of plasmalogen-deficient disorders as they by conversion to a mix of plasmalogens alleviate pathologies resulting from or associated with low plasmalogen levels. In some embodiments, the treatment of plasmalogen-deficient disorders includes raising the level of PE(O)s or PC(O)s in a subject’s plasma or tissues.[000320] In some embodiments, a composition as defined herein is provided for use in increasing the level of PE(O)s and / or PC(O)s in a subject, for example in the subject’s plasma and / or tissue.[000321] In some embodiments, the plasmalogen-associated disorder is selected from the group consisting of a metabolic disorder, a neurological disorder, an inflammatory disorder, a cardiovascular disorder, a peroxisomal disorder, and a neonatal disorder.[000322] In some embodiments, the plasmalogen-associated disorder is selected from the group consisting of a metabolic disorder, a neurological disorder, an inflammatory disorder, a cardiovascular disorder, a peroxisomal disorder, a neonatal disorder, neonatal development, and insufficient neonatal development.Subjects[000323] In some embodiments, the composition of the present disclosure is administered to a subject, wherein the subject is a neonate, infant, child, adolescent, or adult.[000324] In some embodiments, the subject is an adult.[000325] In some embodiments, the subject is an infant.Infants[000326] In some embodiments, the present disclosure provides a composition for use in increasing the levels of plasmalogens in an infant, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000327] In some embodiments, the present disclosure provides use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a composition for use in increasing the levels of plasmalogens in an infant.[000328] In some embodiments, the present disclosure provides a method of increasing the levels of plasmalogens in an infant, comprising adding an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof to a nutritional formulation for the infant.[000329] In some embodiments, administration of the composition improves the immunity of the infant.[000330] In some embodiments, administration of the composition reduces inflammation in the infant.[000331] In some embodiments, administration of the composition reduces the number of infections in the infant.[000332] In some embodiments, administration of the composition improves neurodevelopment in the infant.[000333] As supported at least by Examples 17, 18 and 20C, administration of the composition of the present disclosure to a subject is beneficial in treatment of peroxisomal disorders, treatment of and / or prevention of neurodevelopment disorders, and development of infant immune systems.[000334] In some embodiments, administration of the composition prevents, treats and / or alleviates a peroxisomal disorder, prevents and / or ameliorates neurodevelopment disorders, and assists in development of infant immune systems.[000335] In some embodiments, the composition is administered to the subject for treatment of peroxisomal disorders, wherein the composition comprises LPC(O) and / or LPE(O) with alkyl chains of 16 or 18 in length. In some embodiments, the LPE(O) or LPC(O) is a mixture of 55:45 C16.0 to C18.0 LPE(O). In some embodiments, the LPE(O) or LPC(O) is a50:50 mixture of C16.0 to C18.0 LPE(O). In some embodiments the LPE(O) or LPC(O) is a 2:2: 1 mixture of 16.0, 18.0, 18.1 LPE(O) or LPC(O).[000336] In some embodiments, the composition is administered for treatment of Rhizomelic chondrodysplasia punctata or Zellweger Syndrome, wherein the subject is an infant or toddler characterized by an inability to synthesize a sufficient amount of plasmalogens in their peroxisomes.[000337] In some embodiments, the composition is administered in a daily dosage of eg 0.2 mg / kg to 25 mg / kg / day, or 0.1-4000 mg LPC(O) equivalents per day.[000338] In some embodiments, the composition is administered to the subject for treatment and / or prevention of neurodevelopment disorders, and development of infant immune systems, wherein the composition comprises LPC(O) and / or LPE(O) with alkyl chains of 16 or 18 in length. In some embodiments, the LPE(O) or LPC(O) is a mixture of 55:45 C16.0 to C18.0 LPE(O). In some embodiments, the LPE(O) or LPC(O) is a 50:50 mixture of C16.0 to C18.0 LPE(O). In some embodiments the LPE(O) or LPC(O) is a 2:2: 1 mixture of 16.0, 18.0, 18.1 LPE(O) or LPC(O). In some embodiments the LPE(O) or LPC(O) is a 40:30:30 mixture of 16.0, 18.0, 18.1 LPE(O) or LPC(O). In some embodiments, AKGs are included with the LPX(O)s. In some embodiments, polyunsaturated fatty acids such as EP A, ARA and / or DHA are included with the LPX(O)s for neurodevelopment. In some embodiments, the dosage of 250-500 mg / day fatty acids is included. In some embodiments, 10-12 mg / kg / day is included.[000339] In some embodiments, an infant formula comprising the composition, such as a fortified infant formula comprising the composition is provided for treatment and / or prevention of developmental delays or frequent illness or inflammation, wherein the subject is an infant or toddler, for example characterized by an inability to obtain enough nutritional supplementation via nursing. In some embodiments, the composition is administered to a pregnant woman (prenatal) or a lactating woman, for example a lactating woman producing insufficient amounts of plasmalogen in their breast milk via their normal diet.[000340] In some embodiments, an infant formula is provided comprising the composition in amounts of eg 35 - 442 uM, and optionally with eg about 110-805 uM AKGs. In some embodiments, a lactating or pre-natal woman is supplemented with the equivalent human dose to 1.4-5 mg of LPX(O) and optionally 1-3.3 mg of AKG per mouse per day; or approximately 200 - 1500 mg / day per woman.Metabolic disorders[000341] In some embodiments, the composition of the present disclosure is administered to a subject for treatment of a metabolic disorder.[000342] Decreased plasmalogen levels may contribute to impaired insulin signaling, increased oxidative stress, lipid peroxidation, mitochondrial dysfunction, and chronic low-grade inflammation, all of which are key drivers of metabolic dysfunction. Modulation of plasmalogen levels by administration of a composition of the present disclosure enhance plasmalogen levels to inter alia restore membrane integrity, improve metabolic homeostasis, and reduce oxidative and inflammatory stress, thereby offering therapeutic potential for the treatment or prevention of metabolic disorders, for example the specific metabolic disorders disclosed herein.[000343] In some embodiments, the metabolic disorder is selected from the group consisting of: a liver disease, diabetes, obesity, a lipid disorder, metabolic syndrome, a cardiovascular disorder, and a mitochondrial disorder.[000344] In some embodiments, the metabolic disorder is obesity and / or type-2-diabetes.Liver disease[000345] In some embodiments, a method is provided for increasing liver health of a subject, comprising administering the composition of the present disclosure to the subject. [000346] In some embodiments, a method is provided for treatment of dyslipidemia in a subject, comprising administering the composition of the present disclosure to the subject.[000347] In some embodiments, the liver disease is selected from the group consisting of: non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver steatosis, hepatitis, liver fibrosis, cirrhosis, and liver cancer.[000348] In some embodiments, the liver disease is non-alcoholic fatty liver disease (NAFLD).[000349] In some embodiments, the liver disease is non-alcoholic steatohepatitis (NASH).[000350] In some embodiments, the NAFLD is progressive with increased steatosis, increased inflammation, increased fibrosis, or increased cirrhosis.[000351] In some embodiments, the NAFLD is stable with preserved liver function.[000352] In some embodiments, the NAFLD is metabolic dysfunction-associated steatotic liver disease (MASLD).[000353] In some embodiments, the composition comprises a lysoalkylphosphatidylethanolamine, LPE(O). In some embodiments, the composition comprises C18.0 LPE(O). In some embodiments, the composition comprises C16.0 LPE(O). In some embodiments the composition comprises Cl 8.0 LPE(O) In some embodiments the composition comprises a mixture of 2 or more of C18.0, C16.0, and C18.1 LPE(O). In some embodiments the composition comprises a mixture of 55% C16.0 / 45% C18.0 LPE(O). In some embodiments the composition comprises a mixture C16.0 and C18.0 LPE(O), wherein composition comprises from 30% to 70% C16.0 the balance being C18.0 LPE(O). In some embodiments the composition comprises a mixture C16.0 and C18.0 LPE(O), wherein composition comprises from 30% to 70% C16.0 the balance being C18.1 LPE(O).[000354] In some embodiments the composition comprises a mixture C16.0 and C18.0 LPE(O), wherein composition comprises from 30% to 70% C18.0 the balance being C18.1 LPE(O).[000355] In some embodiments the composition comprises a mixture of 50% C16.O / 50% C18.0 LPE(O). In some embodiments the composition comprises 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio. In some embodiments the composition comprises 16:0, 18:0, and 18: 1 at a 40:30:30 ratio. [000356] In some embodiments, the composition comprises a lysoalkylphosphatidylcholine, LPC (O). In some embodiments, the composition comprises a C18.0 LPC(O), C18.1 LPC(O), C16.0 LPC(O), or a mixture thereof.[000357] In some embodiments, the composition additionally comprises AKGs.[000358] In some embodiments, the composition additionally comprises omega 3 fatty acids. In some embodiments, the omega 3 fatty acids are DHA or EPA or a combination thereof, used at a dose of 0.25-6.8 grams / day.[000359] As supported at least by Examples 10 and 21 and Figures 25, 26, and 96, the administration of the composition results in an increased level of PE(O)s and / or PC(O)s in plasma and neural-like cells.[000360] In some embodiments, the treating, preventing, or protecting against the one or more symptoms of liver disease comprises improvements in liver function.[000361] In some embodiments, the treating, preventing, or protecting against liver disease comprises treating, preventing, or protecting against liver steatosis, hepatitis, liver fibrosis, or liver cirrhosis.[000362] In some embodiments, the treating, preventing, or protecting against the liver disease results in improvements in the liver function based upon changes in liver mass, liver lipids (e.g., triglyceride), expression of markers of liver fibrosis (e.g., Collal), liver inflammation (e.g., TNF alpha), and fatty acid oxidation gene expression (e.g., CPTla, Acoxl) liver imaging, blood metabolic panels, or blood liver protein levels, as shown at least in Example 10.[000363] In some embodiments, treatment of the subject with LPE(O) results in >50% improvement in liver cardiolipin levels, 17% reduction in liver mass, and >30% reduction in visceral adipose tissue mass as compared to untreated subjects on a high fat diet as shown in FIGs. 70-71 and FIG. 76.[000364] In some embodiments, the liver function is determined by serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), C reactive protein (CRP), triglyceride (TG), and HDL-C, LDL-C and total cholesterol.[000365] In some embodiments, the liver inflammation is determined by serum and hepatic expression of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin-1 (IL-1) levels.[000366] In some embodiments, treating the liver disease comprises improvements in liver steatosis, liver inflammation (i.e., hepatitis), liver fibrosis, cirrhosis, or liver metabolism.[000367] In some embodiments, treating the liver disease comprises an improvement in of serum levels of plasmalogens (e.g., lyso species), phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol), sphingolipids (e.g., ceramides, glycosphingolipids and sphingomyelins), glycerolipids (e.g., diacyl- and tri acylglycerols), cholesterol, cholesterol esters, and free fatty acids.[000368] In some embodiments, the liver disease is measured by imaging to determine the extent of liver remodelling associated with steatosis, fibrosis, and cirrhosis.[000369] In some embodiments, the composition is administered in a daily dosage of about 1-100 mg / kg / day, e.g. from about 1-5, about 5-10, about 10-15, about 15-20, about 20-30, about 30-40, about 40-50, about 50-75, or about 75-100 mg / kg / day.[000370] In some embodiments, the daily dosage is provided with respect to combined dose of plasmalogen precursors in the composition.Diabetes[000371] In some embodiments, the present disclosure provides a composition for use in treating, preventing, or protecting against diabetes, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000372] In some embodiments, the present disclosure provides a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating, preventing, or protecting against diabetes.[000373] In some embodiments, the present disclosure provides a method of treating, preventing, or protecting against diabetes in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000374] In some embodiments, a method is provided for increasing insulin sensitivity and / or decreasing insulin resistance in a subject, comprising administering the composition of the present disclosure to the subject.[000375] In some embodiments, the diabetes is type II diabetes.[000376] In some embodiments, the diabetes is diagnosed in a subject with metabolic syndrome.[000377] In some embodiments, the treating, preventing, or protecting against diabetes comprises treating, preventing, or protecting against one or more symptoms of diabetes.[000378] In some embodiments, the one or more symptoms of diabetes include high blood glucose, insulin resistance, cardiovascular disease, diabetic neuropathy, diabetic nephropathy, or diabetic retinopathy.[000379] In some embodiments, the one or more symptoms of diabetes includes high blood glucose.[000380] In some embodiments, the diabetes is progressive with increased insulin resistance.[000381] In some embodiments, the diabetes is stable with preserved insulin sensitivity.[000382] In some embodiments, treating the one or more symptoms of diabetes comprises improvements in insulin sensitivity and / or reduced glucose levels.[000383] In some embodiments, treatment with 0.025% - 0.125% LPE(O) of diet lowers the insulin level of a high fat diet in a subject as shown in FIG. 78. In some embodiments,treatment lowers the HOMA-insulin resistance score of a subject as shown in FIG. 79, or restores hepatic insulin signalling, and / or regulation of glucose homeostasis in a subject. In some embodiments, expression of lrs2 is upregulated and expression of G6pc is downregulated as shown in FIGs. 80-81. In some embodiments, visceral adipose mass is reduced as shown in FIG. 71.[000384] In some embodiments, treatment of LPE(O) 16.0 and 18.0 mixtures of approximately 10.8 mg / kg / day is used.[000385] In some embodiments, treating diabetes comprises reversing or reducing cardiovascular disease, diabetic neuropathy, diabetic nephropathy, diabetic retinopathy.[000386] In some embodiments, reversing or reducing diabetic retinopathy comprises reducing or preventing the development of retinal microaneurysms.[000387] In some embodiments, the treating diabetes comprises normalizing serum levels of C reactive protein (CRP), triglyceride (TG), and HDL-C, LDL-C and total cholesterol.[000388] In some embodiments, treating the diabetes comprises an improvement in of serum levels of plasmalogens (e.g., lyso species), phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol), sphingolipids (e.g., ceramides, glycosphingolipids and sphingomyelins), glycerolipids (e.g., diacyl- and tri acylglycerols), cholesterol, cholesterol esters, and free fatty acids.[000389] In some embodiments, the composition is administered in a daily dosage of about 1-100 mg / kg / day, e.g. from about 1-5, about 5-10, about 10-15, about 15-20, about 20-30, about 30-40, about 40-50, about 50-75, or about 75-100 mg / kg / day.[000390]Obesity and related disorders[000391] In some embodiments, the composition of the present disclosure is administered to a subject for treatment of obesity or an obesity-related disorder.[000392] In some embodiments, the present disclosure provides a use for preventing weight gain and / or promoting weight loss, by administering the composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000393] In some embodiments, the present disclosure provides use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for preventing weight gain and / or promoting weight loss.[000394] In some embodiments, the present disclosure provides use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for reducing fat mass and / or promoting lean muscle retention.[000395] In some embodiments, the present disclosure provides use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for reducing triglycerides, reducing total cholesterol, and / or increasing HDL to LDL cholesterol ratio.[000396] In some embodiments, the present disclosure provides a method of preventing weight gain, reducing fat mass, increasing lean mass, reducing triglycerides, reducing total cholesterol, increasing HDL to LDL ratio, and / or promoting weight loss in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000397] In some embodiments, the composition comprises LPE(O).[000398] In some embodiments, the composition additionally comprises AKGs.[000399] As supported at least by Example 10 and 19B, administration of the composition of the present disclosure to a subject is beneficial in treatment of dyslipidemia.[000400] In some embodiments, treatment of a subject lowers serum cholesterol by about 13% and / or triglyceride levels by about 19% as shown in FIGs 73-74.[000401] Accordingly, in some embodiments, a composition as defined herein is provided for lowering serum cholesterol levels and / or triglyceride levels, for example lowering serum cholesterol levels of from 10 to 40%, such as about 13%, and / or lowering triglyceride levels by at least 15%, such as from 15% to 40%, such as about 19%.[000402] In some embodiments, a GLP-1 receptor agonist, such as semaglutide is administered to the subject prior to, concomitantly with, or subsequent to the composition of the present disclosure. In some embodiments, the present disclosure provides a method for preventing lean body mass loss during GLP-1 treatment and reduces fat mass accumulation on a high fat diet.[000403] In some embodiments, the composition is administered to the subject following cessation of treatment with a GLP-1 receptor agonist, such as semaglutide.[000404] In some embodiments, the composition comprises at least LPE(O), such as LPE(O) 50 wt% 16.0 / 18.0, administered to the subject, for example the subject suffering from obesity or an obesity related disorder of 5 mg / kg / day to 50 mg / kg / day, such as from 5 mg / kg / day to 6 mg / kg / day, such as from 6 mg / kg / day to 7 mg / kg / day, such as from 7 mg / kg / day to8 mg / kg / day, such as from 8 mg / kg / day to 9 mg / kg / day, such as from 9 mg / kg / day to10 mg / kg / day, such as from 10 mg / kg / day to 11 mg / kg / day, such as from 11 mg / kg / day to12 mg / kg / day, such as from 12 mg / kg / day to 13 mg / kg / day, such as from 13 mg / kg / day to14 mg / kg / day, such as from 14 mg / kg / day to 15 mg / kg / day, such as from 15 mg / kg / day to16 mg / kg / day, such as from 16 mg / kg / day to 17 mg / kg / day, such as from 17 mg / kg / day to 18 mg / kg / day, such as from 18 mg / kg / day to 19 mg / kg / day, such as from 19 mg / kg / day to20 mg / kg / day, such as from 20 mg / kg / day to 21 mg / kg / day, such as from 21 mg / kg / day to 22 mg / kg / day, such as from 22 mg / kg / day to 23 mg / kg / day, such as from 23 mg / kg / day to 24 mg / kg / day, such as from 24 mg / kg / day to 25 mg / kg / day, such as from 25 mg / kg / day to 26 mg / kg / day, such as from 26 mg / kg / day to 27 mg / kg / day, such as from 27 mg / kg / day to28 mg / kg / day, such as from 28 mg / kg / day to 29 mg / kg / day, such as from 29 mg / kg / day to 30 mg / kg / day, such as from 30 mg / kg / day to 31 mg / kg / day, such as from 31 mg / kg / day to 32 mg / kg / day, such as from 32 mg / kg / day to 33 mg / kg / day, such as from 33 mg / kg / day to34 mg / kg / day, such as from 34 mg / kg / day to 35 mg / kg / day, such as from 35 mg / kg / day to 36 mg / kg / day, such as from 36 mg / kg / day to 37 mg / kg / day, such as from 37 mg / kg / day to 38 mg / kg / day, such as from 38 mg / kg / day to 39 mg / kg / day, such as from 39 mg / kg / day to40 mg / kg / day, such as from 40 mg / kg / day to 41 mg / kg / day, such as from 41 mg / kg / day to 42 mg / kg / day, such as from 42 mg / kg / day to 43 mg / kg / day, such as from 43 mg / kg / day to 44 mg / kg / day, such as from 44 mg / kg / day to 45 mg / kg / day, such as from 45 mg / kg / day to 46 mg / kg / day, such as from 46 mg / kg / day to 47 mg / kg / day, such as from 47 mg / kg / day to48 mg / kg / day, such as from 48 mg / kg / day to 49 mg / kg / day, such as from 49 mg / kg / day to 50 mg / kg / day. In some embodiments, the composition comprises at least one LPE(O), such as LPE(O) 50 wt% 16.0 / 18.0, administered to the subject at about 10 mg / kg / day. In some embodiments, the composition comprises at least one LPE(O), administered to the subject at about 20 mg / kg / day.In some embodiments, the subject is receiving a GLP-1 receptor agonist, such as semaglutide, or has been receiving the GLP-1 receptor agonist prior to treatment with the composition of the present disclosure.[000405] As supported at least by Examples 10 and 11, co-administration of the composition of the present disclosure with to a subject is beneficial in treatment of obesity and type II diabetes, optionally in co-administration with GLP-1 receptor agonist or post-GLP 1 treatment.[000406] In some embodiments, the composition is administered in a daily dosage of from 1 mg / kg to 100 mg / kg / day with respect to LPX(O), eg from about 1-10 mg / kg / day, or about 10- 20 mg / kg / day, or about 20-30 mg / kg, day, or about 30-50 mg / kg / day, or about 50-75 mg / kg / day, or about 75-100 mg / kg / day.Neurological disorders[000407] Alterations in plasmalogen levels have been implicated in the pathogenesis of various neurological disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, autism spectrum disorder, amyotrophic lateral sclerosis, cognitive impairment, and peroxisomal disorders such as Zellweger spectrum disorders and rhizomelic chondrodysplasia punctata. In such conditions, plasmalogen deficiency may disrupt synaptic function, impair myelination, increase vulnerability to oxidative damage, and promote neurodegenerative processes. Modulation of plasmalogen levels by administration of a composition of the present disclosure may enhance neuronal resilience, improve synaptic function, support remyelination, and mitigate neuroinflammation, thereby providing therapeutic benefit for the prevention or treatment of neurological disorders, in particular those associated with plasmalogen deficiency or dysfunction.[000408] In some embodiments, the composition of the present disclosure is administered to a subject for treatment of a neurological disorder. In some embodiments, the composition of the present disclosure is administered to a subject for treatment of a cognitive disease or disorder. [000409] In some embodiments, the neurological disorder is selected from the group consisting of: a neuronal maturation disorder including a peroxisomal disorder, an infant brain development disorder, Zellweger spectrum disorder, rhizomelic chondrodysplasia punctata, and autism spectrum disorder; a neuronal regeneration disorder including multiple sclerosis (MS), and peripheral neuropathy; a cognitive disorder, including Alzheimer’s disease, mild cognitiveimpairment, vascular dementia, and age-related cognitive decline; and a movement disorder, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS).[000410] In some embodiments, the neurological disorder is Alzheimer's disease (AD), Parkinson’s disease (PD), Multiple sclerosis (MS), autism spectrum disorder, and amyotrophic lateral sclerosis (ALS).[000411] In some embodiments, the peroxisomal disorder is Zellweger spectrum disorder.[000412] In some embodiments, the neurological disorder is selected from the group consisting of Alzheimer’s disease, frontotemporal dementia, and schizophrenia.[000413] As supported at least by Examples 15-22, administration of the composition of the present disclosure to a subject is beneficial in treatment of Alzheimer’s Disease, Parkinson’s Disease, Peroxisomal Disease, neurodevelopment, neural regeneration, neural inflammation, and multiple sclerosis.[000414] In some embodiments, the composition is administered to the subject for treatment of a movement disorder, wherein the composition comprises at least one LPE(O). In some embodiments, the movement disorder is Parkinson’s disease or Multiple Sclerosis.[000415] In some embodiments, the composition is administered for treatment of a cognitive disorder wherein the cognitive disorder is Alzheimer’s Disease, dementia, Lewy -body dementia, or Parkinson’s disease.[000416] In some embodiments, the composition is administered in a daily dosage of, e.g. from 1 mg / kg to 100 mg / kg / day. In some embodiments, the composition is administered at a dose of 1-15 mg / kg / day. In some embodiments, the composition is administered at 12.5-250 mg / kg / day. In some embodiments the composition is administered at about 1-5, 6-10, 11-13, 14- 16, 17-18, 19-20, 21-22, 23-24, 25-26, 27-28, 29-30, 31-35, 36-40, 41-50, 51-74, 75-100 mg / kg / day. In some embodiments, the composition further comprises one or more omega-3 fatty acids, such as DHA, for example wherein the one or more fatty acids are administered to the subject at a dose of from 1 to 10 mg / kg / day. In some embodiments, the composition comprises DHA at a dosage of 2-60 mg / kg / day. In some embodiments, the composition comprises PE(O) at a dosage of 2-35 mg / kg / day. In some embodiments, an omega-6 fatty acid such as ARA is administered for cognition and neurological health at a dose of about 80-240 mg / day.Alzheimer's disease[000417] In some embodiments, a composition is provided for use in treating a cognitive disease or disorder, such as Alzheimer’s disease, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000418] In some embodiments, the present disclosure provides a use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating a cognitive disease or disorder, such as Alzheimer’s disease.[000419] In some embodiments, a method of treating a cognitive disease or disorder is provided, such as Alzheimer’s disease, in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000420] In some embodiments, the cognitive disease or disorder is Alzheimer’s disease.[000421] In some embodiments, treating Alzheimer’s disease comprises reducing the symptoms associated with Alzheimer’s disease.[000422] In some embodiments, treating Alzheimer’s disease comprises reducing a level of at least one biomarker in the subject. In some embodiments, the biomarkers are selected from blood biomarkers, cerebrospinal fluid biomarkers, MRI scans, PET scans, hippocampal volume, brain shrinkage, brain glucose metabolism.[000423] In some embodiments, the biomarkers are blood biomarkers or CSF biomarkers.[000424] In some embodiments, the blood biomarkers or the CSF biomarkers are selected from beta-amyloid 42, tau, and phospho-tau.[000425] In some embodiments, the symptoms associated with Alzheimer’s disease are determined using the Global Deterioration Scale.[000426] In some embodiments, the stage of symptoms is reduced on the Global Deterioration Scale.[000427] In some embodiments, treating Alzheimer’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Alzheimer’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.[000428] In some embodiments, reducing the symptoms associated with Alzheimer’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Alzheimer’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.[000429] In some embodiments, the composition for use in the treatment additionally comprises one or more of an (N)-methyl-D-aspartate receptor antagonist, selective serotonin reuptake inhibitor or an acetylcholinesterase inhibitor.[000430] In some embodiments, the acetylcholinesterase inhibitor is donepezil, rivastigmine, or galantamine.[000431] In some embodiments, the (N)-methyl-D-aspartate receptor antagonist is memantine.[000432] In some embodiments, the selective serotonin reuptake inhibitor is citalopram, escitalopram, paroxetine, or sertraline.Peroxisomal disorders[000433] In some embodiments, a composition is provided for use in treating a peroxisomal disorder and / or symptoms thereof, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000434] In some embodiments, the present disclosure provides the use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating a peroxisomal disorder.[000435] In some embodiments, a method of treating a peroxisomal disorder and / or symptoms thereof in a subject in need thereof is provided, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000436] In some embodiments, treating a peroxisomal disorder and / or symptoms thereof comprises treating rhizomelic chondrodysplasia punctata, Zellweger spectrum disorders, Refsum Disease, X-Linked Adrenoleukodystrophy.[000437] In some embodiments, Zellweger spectrum disorder comprises Zellweger Syndrome, Neonatal Adrenoleukodystrophy, Refsum Disease and Infantile Refsum Disease. [000438] In some embodiments, treating a peroxisomal disorder and / or symptoms thereof comprises treating rhizomelic chondrodysplasia punctata, or Zellweger.[000439] In some embodiments, treating a peroxisomal disorder and / or symptoms thereof comprises treating the symptoms associated with a peroxisomal disease.[000440] In some embodiments, treating the symptoms associated with a peroxisomal disorder comprises reducing the symptoms associated with a peroxisomal disorder.[000441] In some embodiments, treating a peroxisomal disorder and / or symptoms thereof comprises reducing a level of at least one biomarker in the subject.[000442] In some embodiments, the biomarkers are selected from blood biomarkers, cerebrospinal fluid biomarkers, single photon emission computed tomography scan, MRI scan, CT scan.[000443] In some embodiments, the biomarkers are cortical and cerebellar migrational abnormalities, central white-matter demyelination, blood biomarkers or CSF.[000444] In some embodiments, the blood biomarkers or the CSF biomarkers are very- long-chain fatty acids, phytanic acid, pipecolic acids, and deficient synthesis of plasmalogens, elevated protein levels.[000445] In some embodiments, reducing the level of the biomarker comprises one or more of reducing the levels of phytanic acid in the subject.[000446] In some embodiments, the symptoms associated with peroxisomal disorders are nerve damage, retinopathy, hearing loss, anosmia, spastic movements, and changes in the bone and skin, demyelination, seizures, hypotonia, enlarged liver, hepatic cysts, cataracts, hearing loss, bradykinesia, and weakness, numbness, and pain in the hands and feet.[000447] In some embodiments, reducing the symptoms comprises reducing seizure severity, reducing the frequency of seizure, slowing the progression of retinopathy, slowing the progression of hearing loss, slowing the progression of anosmia, reducing the frequency of spastic movements, slowing the progression of demyelination.[000448] In some embodiments, treating peroxisomal disorder and / or symptoms comprises the steps of:(a) determining the level of one or more biomarkers of a peroxisomal disorder from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.[000449] In some embodiments, treating the symptoms associated with a peroxisomal disorder comprises the steps of:(a) determining the level of one or more biomarkers of a peroxisomal disorder from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.Parkinson's disease[000450] In some embodiments, the present disclosure provides a composition for use in treating a movement or motor disorder, such as Parkinson’s disease, and / or symptoms thereof, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000451] In some embodiments, the present disclosure provides a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating a movement or motor disorder, such as Parkinson’s disease, and / or symptoms thereof.[000452] In some embodiments, the present disclosure provides a method of treating a movement or motor disorder, such as Parkinson’s disease, and / or symptoms thereof in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000453] In some embodiments, treating a movement or motor disorder, such as Parkinson’s disease and / or symptoms thereof comprises treating Parkinson’s disease. [000454] In some embodiments, treating a movement or motor disorder, such asParkinson’s disease and / or symptoms thereof comprises treating the symptoms associated with Parkinson’s disease.[000455] In some embodiments, treating the symptoms associated with Parkinson’s disease comprises reducing the symptoms associated with Parkinson’s disease.[000456] In some embodiments, treating a movement or motor disorder, such as Parkinson’s disease and / or symptoms thereof comprises reducing a level of at least one biomarker in the subject.[000457] In some embodiments, the biomarkers are selected from blood biomarkers, cerebrospinal fluid biomarkers, single photon emission computed tomography scan, MRI scan, CT scan.[000458] In some embodiments, the biomarkers are loss of structure in the substantia nigra, blood biomarkers or CSF biomarkers.[000459] In some embodiments, the blood biomarkers or the CSF biomarkers are a- synuclein, neurofilament light chain, glial fibrillary acidic protein, 0-amyloid 1-42, tau, p-tau, or YKL-40.[000460] In some embodiments, the symptoms associated with Parkinson’s disease are tremor, bradykinesia, muscle stiffness, balance problems, anosmia, nerve pain, urinary incontinence, constipation, erectile dysfunction, sexual dysfunction, dizziness, blurred vision, hyperhidrosis, dysphagia, drooling, insomnia, depression, anxiety, dementia, or Lewy -body dementia.[000461] In some embodiments, the stage of symptoms is reduced on the Hoehn-Yahr staging system or the Movement Disorder Society -Unified Parkinson’s Disease Rating Scale. [000462] In some embodiments, treating the Parkinson’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Parkinson’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.[000463] In some embodiments, treating the symptoms associated with Parkinson’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Parkinson’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined herein.[000464] In some embodiments, the composition is a meal replacement therapy. In some embodiments, the meal replacement therapy is formulated for an adult subject.[000465] In some embodiments, the composition as defined herein additionally comprises one or more of levodopa, a dopamine agonist, a monoamine oxidase-B inhibitor or a catechol-O- methyltransferase inhibitor.[000466] In some embodiments, the dopamine agonist is pramipexole, or ropinirole.[000467] In some embodiments, the monoamine oxidase-B inhibitor is rasagiline, selegiline, or safinamide.[000468] In some embodiments, the catechol-O-methyltransferase inhibitor is entacapone, or opicapone.Multiple sclerosis[000469] In some embodiments, the present disclosure provides composition for use in treating multiple sclerosis, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000470] In some embodiments, the present disclosure provides use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating multiple sclerosis.[000471] In some embodiments, the present disclosure provides treatment of multiple sclerosis in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000472] In some embodiments, treating multiple sclerosis comprises treating one or more symptoms of the multiple sclerosis.[000473] In some embodiments, the multiple sclerosis is progressive with increased severity of one or more symptoms of multiple sclerosis.[000474] In some embodiments, the multiple sclerosis is stable with no new symptoms or worsening symptoms of multiple sclerosis.[000475] In some embodiments, treating the one or more symptoms of multiple sclerosis comprises improvements in daily quality of life.[000476] In some embodiments, the one or more symptoms of multiple sclerosis comprise: neuroinflammation of the central nervous system, numbness or weakness in one or more limbs, tingling, electric- shock sensations, lack of coordination, unsteady gait, inability to walk, loss of vision, double vision, blurry vision, vertigo, fatigue, slurred speech, cognitive problems, mood disturbances, or dysregulation of gastrointestinal and genitourinary function.[000477] In some embodiments, treating multiple sclerosis results in improvements in mobility of the subject.[000478] In some embodiments, treating multiple sclerosis results in reduced neuroinflammation of the central nervous system.[000479] In some embodiments, treating multiple sclerosis results in improved cognitive function.[000480] In some embodiments, treating multiple sclerosis results in improved vision (e.g., reduced blurry vision and double vision).[000481] In some embodiments, treating multiple sclerosis results in improved gastrointestinal and genitourinary function.[000482] In some embodiments, treating multiple sclerosis reduces the size and number of meningeal and parenchymal inflammatory foci.[000483] In some embodiments, treating multiple sclerosis comprises an improvement in serum levels of plasmalogens (e.g., lyso species), phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol), sphingolipids (e.g., ceramides, glycosphingolipids and sphingomyelins), glycerolipids (e.g., diacyl- and tri acylglycerols), cholesterol, cholesterol esters, and free fatty acids.[000484] In some embodiments, the composition comprises LPE(O) C16:0 / LPE(O) C18:0 and is administered to the subject suffering from multiple sclerosis.[000485] In some embodiments, the composition comprises about 55% LPE(O) C16:0 and about 45% LPE(O) Cl 8:0.[000486] As demonstrated in Example 19, the composition of the present disclosure shows potential in lowering the frequency of occurrences and / or intensity of symptoms in relapsing / remitting cases of MS.[000487] As supported at least by Example 19B, administration of the composition of the present disclosure to a subject is beneficial in delaying the onset of MS symptoms and / or improving recovery time from the MS symptoms.[000488] In some embodiments, the composition is administered to the subject for treatment of MS, wherein the composition comprises one or more LPE(O)s and is administered to the subject in combination with fmgolimod. In some embodiments, the composition comprises an effective amount of at least one compound of Formula (I-A) of at least about 19 mg / kg / day. In some embodiments, the fmgolimod is present at about 0.3-10 mg / kg / day. In some embodiments the effective amount of the composition comprising at least one compound of Formula (I-A) is at least about 1-4, 5-10, 11-13, 14-16, 17-19, 20-22, 23-25, 26-28, 29-31, 32-35, 36-40, 41-45, 46-50, 51-74, 75-100 mg / kg / day. In some embodiments, the composition is administered in a daily dosage from about 1 mg / kg to 100 mg / kg / day, or about 5-75 mg / kg / day, or about 7-50 mg / kg / day, or about 10-30 mg / kg / day, or about 10-20 mg / kg / day.[000489] In some embodiments, the at least one compound of Formula (I-A) is about a 50:50 mixture of LPE(O) C16.0:C18.0. In some embodiments, the composition comprises about a 2:2: 1 mixture of C16.0, C18.0, and C18.1 LPE(O)s. In some embodiments the composition comprises a 40:30:30 mixture of C16.0 / C18.0 / C18.1 LPE(O).Inflammatory disorders[000490] In some embodiments, the composition of the present disclosure is administered to a subject for treatment of an inflammatory disorder.[000491] The inflammatory disorders of the present disclosure can be traditional inflammatory disorders or can be other disorders that have e.g. a metabolic and / or neuronal origin but present with inflammation.[000492] In some embodiments, the inflammatory disorder is selected from the group consisting of: an autoimmune disease, such as rheumatoid arthritis (RA), lupus, psoriasis, inflammatory bowel disease (IBD), multiple sclerosis (MS), and ankylosing spondylitis; a cardiovascular disease; a gastrointestinal disorder, such as inflammatory bowel disease (IBD), Crohn’s disease, and ulcerative colitis (UC); type-2-diabetes; a neurodegenerative disease; and bronchopulmonary dysplasia (BPD).[000493] In some embodiments, the inflammatory disorder is rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), Psoriasis, Asthma, and Chronic Obstructive Pulmonary Disease (COPD).[000494] As supported at least by Example 14 and 19, administration of the composition of the present disclosure to a subject is beneficial in treatment of inflammatory diseases Multiple sclerosis and cardiovascular disease.[000495] In some embodiments, the composition is administered to the subject for treatment of cardiovascular disease, wherein the composition comprises about a 40:30:30 mixture of C16.0 / C18.0 / C18.1 LPE(O)s and / or AKGs.[000496] In some embodiments, the composition is administered for treatment of MS, wherein the composition comprises 55% LPE(O) C16:0 and 45% LPE(O) C18:0.[000497] In some embodiments, the composition is administered in a daily dosage of, e.g. from 1 mg / kg to 100 mg / kg / day. In some compositions, the composition is administered in a daily dosage of, eg, 1-9 mg / kg / day; 10-12 mg / kg / day, 13-15 mg / kg / day, 16-20 mg / kg / day, 21-30 mg / kg / day, 31-50 mg / kg / day, or 75-100 mg / kg / day.In some embodiments, the inflammatory disease is rheumatoid arthritis. In some embodiments, the composition additionally comprises DHA and / or EPA at a dose of 250 mg-3 g / day.Cardiovascular disorders[000498] In some embodiments, the composition of the present disclosure is administered to a subject for treatment of a cardiovascular disorder.[000499] In some embodiments, a method is provided for prevention of cardiovascular disorders in a subject, and / or prevention of heart disease, and / or clogging of arteries.[000500] In some embodiments, a methods is provided for increasing cardiovascular health of a subject, comprising administering a composition as defined herein to the subject.[000501] In some embodiments, a composition is provided for use in treating cardiovascular disease, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.[000502] In some embodiments, the present disclosure provides a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating cardiovascular disease.[000503] In some embodiments, the present disclosure provides method of treating cardiovascular disease in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.[000504] In some embodiments, the cardiovascular disorder is atherosclerosis, coronary artery disease, heart failure, hypertension, arrhythmias, and peripheral artery disease.[000505] In some embodiments, the cardiovascular disorder is acute, e.g. in the acute phase. In some embodiments, the cardiovascular disorder is chronic, e.g. in the chronic phase. [000506] In some embodiments, the cardiovascular disease is selected from atherosclerosis, arteriosclerosis, myocardial infarction, angina pectoris, heart failure, embolism, thrombus, hypertension, acute coronary syndrome, myocardial repair, ischemia reperfusion injury, cardiac remodeling, cardiac arrhythmias, heart failure with preserved ejection fraction, heart failure with reduced ejection fraction, dilated cardiomyopathy and diabetic cardiomyopathy.[000507] In some embodiments, treating cardiovascular disease comprises treating the symptoms of cardiovascular disease.[000508] In some embodiments, the cardiovascular disease is myocardial infarction.[000509] In some embodiments, the cardiovascular disease is heart failure.[000510] In some embodiments, the heart failure is heart failure with reduced ejection fraction.[000511] In some embodiments, the heart failure is heart failure with preserved ejection fraction.[000512] In some embodiments, treating the symptoms of cardiovascular disease comprises improvements in ejection fraction.[000513] In some embodiments, treating cardiovascular disease comprises regulating or lowering blood pressure, inhibiting or minimizing atherosclerotic plaque formation, and reducing or reversing cardiac remodelling.[000514] In some embodiments, the treating the cardiovascular disease results in improvements in the Reynolds Risk score, a blood test, electrocardiogram, echocardiogram, nuclear stress test, carotid ultrasound, abdominal ultrasound, cardiac catheterisation, coronary angiography, ischemia reperfusion injury or exercise stress test.[000515] In some embodiments, the blood test determines the lipid profile of the blood.[000516] In some embodiments, the lipid profile includes one or more of: total cholesterol, LDL (low-density lipoprotein), HDL (high-density lipoprotein), triglycerides, lipoprotein(a), high sensitivity C-reactive protein, homocysteine.[000517] In some embodiments, treating the cardiovascular disease comprises improvements in life span, muscle hypertrophy, contractility, fibrosis, or metabolism.[000518] In some embodiments, treating the cardiovascular disease comprises a reduction in circulating proinflammatory monocytes, fibrosis and neutrophil infiltration.[000519] In some embodiments, the echocardiogram comprises determining the left ventricular (LV) wall thickness, LV global longitudinal strain, chamber volumes, or cardiac function.[000520] In some embodiments, the cardiovascular disease is dilated cardiomyopathy.[000521] In some embodiments, treating the dilated cardiomyopathy comprises a reduction in chest pain, fatigue, breathing difficulties, oedema of the extremities.[000522] In some embodiments, the treatment further comprises the use or administration of one or more alkylglycerols.[000523] In some embodiments, the composition further comprises the one or more alkylglycerols.[000524] In some embodiments, the composition is administered to a subject suffering from Dilated Cardiomyopathy (DCM).[000525] In some embodiments, the composition is administered to a subject who has suffered from heart attack to decrease risk of subsequent heart attacks.Chronic[000526] In some embodiments, the composition increases both PC and PE plasmalogen species with 18:0, 18: 1, and 16:0 fatty alcohol chains in the ventricles and plasma of the Ntg and DCM mice vs. controls (FIG. 82B, 82C). Accordingly, the present disclosure provides a method of increasing PC and PE plasmalogen levels in ventricles and plasma in a subject by administering the composition of the present disclosure to the subject.[000527] In some embodiments, the composition is administered to a subject for treatment of a chronic cardiovascular disorder.[000528] In some embodiments, the composition is administered to a subject for treatment of idiopathic dilated cardiomyopathy, familial dilated cardiomyopathy, peripartumcardiomyopathy, inflammatory dilated cardiomyopathy, heart failure with reduced ejection fraction, chronic heart failure, acute decompensated heart failure, viral myocarditis, autoimmune myocarditis, doxorubicin-induced cardiomyopathy, chemotherapy-related cardiomyopathies, post-myocardial infarction remodeling, ischemic cardiomyopathy, diabetic cardiomyopathy, obesity-related cardiomyopathy, mitochondrial disorders affecting myocardium, muscular dystrophies with cardiac involvement, mitochondrial myopathies with dilated cardiomyopathy features, amyloid cardiomyopathy, dilated cardiomyopathy in dogs, and feline cardiomyopathies. [000529] In some embodiments, the composition is administered to a subject for treatment of idiopathic dilated cardiomyopathy, familial dilated cardiomyopathy, peripartum cardiomyopathy, inflammatory dilated cardiomyopathy, heart failure with reduced ejection fraction, chronic heart failure, doxorubicin-induced cardiomyopathy, chemotherapy-related cardiomyopathies, diabetic cardiomyopathy, obesity-related cardiomyopathy, mitochondrial disorders affecting myocardium, muscular dystrophies with cardiac involvement, mitochondrial myopathies with dilated cardiomyopathy features, and dilated cardiomyopathy in dogs.Acute[000530] In some embodiments, the composition is administered to a subject for treatment of an acute cardiovascular disorder. In some embodiments, the composition is administered to a subject for treatment of ischemia reperfusion injury.[000531] As shown in Example 14, AKG supplementation in a mouse model of IR was associated with attenuated circulating proinflammatory monocytes at 24 hours post IR as compared to chow fed controls.[000532] In some embodiments, the composition is administered to a subject to prevent ischemia reperfusion injury or to decrease the pathological effects resulting from ischemia reperfusion injury.[000533] In some embodiments, the composition is administered to a subject to protect against heart failure and ischemia reperfusion injury.[000534] As supported at least by Example 14, administration of the composition of the present disclosure to a subject is beneficial in treatment during and immediately following a myocardial infarction, for example a 5-20 uM mixture of 40% LPE(O-16:0), 30% LPE(O-18:0), and 30% LPE(O-18: 1) in DMEM with 1% sodium pyruvate and optionally 5,20,80 uM AKGs to rat cardiomyoblasts, human-derived iPSC cardiomyoblasts and 3D cardiac spheroids raisedPE(O) and PE(P) levels, improved contractile function, and raised cardiolipin levels and lowered ROS levels in the mitochondria.[000535] In some embodiments, the composition is administered in a daily dosage of, e.g. from 1 mg / kg / day to 100 mg / kg / day. In some embodiments, the composition is administered in a daily dosage of 2.5-20 mg / kg / day. In some embodiments, the composition further comprises AKGs at a dosage of 1.5-50 mg / kg / day.[000536] In some embodiments, the treatment for cardiac health includes an omega-3 fatty acid such as ALA, DHA, or EPA. In some embodiments, the treatment includes an omega-3 fatty acid such as ALA, DHA, or EPA.Numbered Embodiments - Liver and Obesity1. A composition for use in preventing weight gain and / or promoting weight loss, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.2. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for preventing weight gain and / or promoting weight loss.3. A method of preventing weight gain and / or promoting weight loss in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.4. A composition for use in treating, preventing, or protecting against liver disease, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.5. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating, preventing, or protecting against liver disease.6. A method of treating, preventing, or protecting against liver disease in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.7. The use or method of any one of embodiments 1 to 6, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.8. The use or method of any one of embodiments 1 to 7, wherein n is 2 or 3.9. The use or method of any one of embodiments 1 to 6, wherein Rx is methyl, and n is 3.10. The use or method of any one of embodiments 1 to 9, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.11. The use or method of embodiment 10, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted C14-24 acyl group.12. The use or method of any one of embodiments 1 to 11, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.13. The use or method of embodiment 12, wherein RA is an optionally substituted C14-18 alkyl group, an optionally substituted C14-18 alkenyl group, or an optionally substituted C14-18 acyl group.14. The use or method of embodiment 13, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.15. The use or method of embodiment 14, wherein RA is an optionally substituted C16-18 alkyl group.16. The use or method of embodiment 14, wherein RA is an optionally substituted C16-18 alkenyl group.17. The use or method of embodiment 14, wherein RA is an unsubstituted Ci6 alkyl group.18. The use or method of embodiment 14, wherein RA is an unsubstituted Cis alkyl group.19. The use or method of embodiment 14, wherein RA is an unsubstituted Cis alkenyl group.20. The use or method of any preceding embodiment, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).21. The use or method of any preceding embodiment, wherein the composition comprises a mixture of three compounds of Formula (I-A).22. The use or method of any one of embodiments 1 to 6, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).23. The use or method of embodiment 22, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I- A3).24. The use or method of embodiment 22, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-Al), (I-A2), and (I-A3).25. The use or method of any one of embodiments 22 to 24, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).26. The use or method of any one of embodiments 20 to 22, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of (I-Al), (I-A2), and (I- A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.27. The use or method of embodiment 21, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).28. The use or method of embodiment 27, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).29. The use or method of embodiment 27, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).30. The use or method of embodiment 21, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I-A3).31. The use or method of embodiment 30, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).32. The use or method of embodiment 31, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I-A3).33. The use or method of embodiment 21, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I- A3).34. The use or method of embodiment 33, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).35. The use or method of embodiment 34, wherein the mixture has a molar ratio of from 0.72: 1 of (I-Al) to (I-A3).36. The use or method of embodiment 25, wherein the mixture has a molar percentage of (I- Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.37. The use or method of embodiment 36, wherein the mixture has a molar percentage of (I- Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I-A3) of 32.1%.38. The use or method of embodiment 36, wherein the mixture has a molar ratio of (I-A1):(I- A2):(I-A3) of 1 : 1.7: 1.4.39. The use or method of embodiment 26, wherein the mixture of at least two compounds is a 50:50 mixture.40. The use or method of embodiment 27, wherein the mixture of (I-Al), (I-A2) and (I-A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18: 1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18:1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; or LPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.41. The use or method of embodiment 27, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-Al).42. The use or method of embodiment 27, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A2).43. The use or method of embodiment 27, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A3).44. The use or method of embodiment 27, wherein the mixture of (I-Al), (I-A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).45. The use or method of any one of embodiments 1 to 6, wherein the compound of Formula (I-A) is of the structure (I-A4), (I-A5), or (I-A6).46. The use or method of embodiment 45, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-A4), (I-A5), and (I-A6).47. The use or method of embodiment 45 or embodiment 46, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6).48. The use or method of embodiment 47, wherein the at least one compound is selected from a compound of Formula (I-A4), (I-A5) or (I-A6).49. The use or method of embodiment 45, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6), wherein said mixture of (I-A4), (I-A5), and (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.50. The use or method of embodiment 45, wherein the mixture has a molar ratio of from 1.2:1 to 2.5:1 of (I-A5) to (I-A4).51. The use or method of embodiment 50, wherein the mixture has a molar ratio of from 1.5:1 to 2.1:1 of (I-A5) to (I-A4).52. The use or method of embodiment 51 , wherein the mixture has a molar ratio of 1.7: 1 of (I-A5) to (I-A4).53. The use or method of embodiment 45, wherein the mixture has a molar ratio of from 0.9:1 to 1.7:1 of (I-A5) to (I-A6).54. The use or method of embodiment 53, wherein the mixture has a molar ratio of from 1 : 1 to 1.5:1 of (I-A5) to (I-A6).55. The use or method of embodiment 54, wherein the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6).56. The use or method of embodiment 45, wherein the mixture has a molar ratio of from 0.5:1 to 1:1 of (I-A4) to (I-A6).57. The use or method of embodiment 56, wherein the mixture has a molar ratio of from 0.6:1 to 0.9:1 of (I-A4) to (I-A6).58. The use or method of embodiment 57, wherein the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6).59. The use or method of embodiment 47, wherein the mixture has a molar percentage of (I- A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 26.8% to 37.4%.60. The use or method of embodiment 59, wherein the mixture has a molar percentage of (I- A4) of 24.8%, a molar percentage of (I-A5) of 42.4%, and a molar percentage of (I-A6) of 32.8%.61. The use or method of embodiment 59, wherein the mixture has a molar ratio of (I-A4):(I- A5):(I-A6) of 1:1.7: 1.3.62. The use or method of embodiment 49, wherein the mixture of the at least two compounds is a 50:50 mixture.63. The use or method of embodiment 50, wherein the mixture of (I-A4), (I-A5) and (I-A6) is selected from:LPE(O-16:0) 26.8% + LPE(O-18:0) 46.1% + LPE(O-18:1) 27.1%;LPE(O-16:0) 46% + LPE(O-18:0) 21% + LPE(O-18:1) 33%;LPE(O-16:0) 42% + LPE(O-18:0) 51% + LPE(O-18:1) 7%;LPE(O-16:0) 62% + LPE(O-18:0) 23.9% + LPE(O-18:1) 14.1%;LPE(O-16:0) 19.8% + LPE(O-18:0) 66% + LPE(O-18:1) 14.2%;LPE(O-16:0) 32.5% + LPE(O-18:0) 39.6% + LPE(O-18:1) 27.9%; or LPE(O-16:0) 34.1% + LPE(O-18:0) 41.5% + LPE(O-18:1) 24.4%.64. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A4).65. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A5).66. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A6).67. The use or method of any one of embodiments 1 to 66, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 4000 mg per day.68. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 2000 mg per day.69. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 1600 mg per day.70. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of 400 mg, 800 mg, or 1600 mg per day.71. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of 200 mg per day.72. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 100 mg per day.73. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of 25 mg, 50 mg, or 100 mg per day.74. The use or method of embodiment 67, wherein the compound of Formula (I-A) is administered in a dose of 30 mg, 100 mg, or 300 mg per day.75. The use or method of any one of embodiments 1 to 74, wherein the composition is a pharmaceutical composition.76. The use or method of any one of embodiments 1 to 74, wherein the composition is a pharmaceutical formulation.77. The use or method of any one of embodiments 1 to 74, wherein the composition is a food.78. The use or method of any one of embodiments 1 to 74, wherein the composition is dietary supplement.79. The use or method of any one of embodiments 1 to 74, wherein the composition is a medicinal food.80. The use or method of any one of embodiments 1 to 79, wherein the composition is suitable for oral administration.81. The use or method of embodiment 80, wherein the oral administration form is a tablet, a capsule, a solution, a mouthwash, a suspension, a powder, a gum, a confectionary, a lozenge, a sublingual delivery system, or a rapid-melt formulation.82. The use or method of any one of embodiments 1 to 81, wherein the composition comprises at least one of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an antioxidant, an antifoaming agent, or a diluent.83. The use or method of embodiment 82, wherein the composition comprises at least one solubilizing agent.84. The use or method of embodiment 83, wherein the solubilizing agent is selected from the group consisting of carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, food grade solvents, phospholipids, DMSO, ethanol, ethyl acetate, and isopropanol.85. The use or method of any one of embodiments 4 to 84, wherein the liver disease is selected from non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver steatosis, hepatitis, liver fibrosis, cirrhosis, and liver cancer.86. The use or method of any one of embodiments 4 to 85, wherein the treating, preventing, or protecting against liver disease comprises treating, preventing, or protecting against one or more symptoms of the liver disease.87. The use or method of any one of embodiments 4 to 86, wherein the liver disease is nonalcoholic fatty liver disease (NAFLD).88. The use or method of any one of embodiments 4 to 86, wherein the liver disease is nonalcoholic steatohepatitis (NASH).89. The use or method of embodiment 87, wherein the NAFLD is progressive with increased steatosis, increased inflammation, increased fibrosis, or increased cirrhosis.90. The use or method of embodiment 87, wherein the NAFLD is stable with preserved liver function.91. The use or method according to embodiment 86, wherein the treating, preventing, or protecting against the one or more symptoms of liver disease comprises improvements in liver function.92. The use or method of any one of embodiments 4 to 91, wherein the treating, preventing, or protecting against liver disease comprises treating, preventing, or protecting against liver steatosis, hepatitis, liver fibrosis, or liver cirrhosis.93. The use or method of any one of embodiments 4 to 91, wherein the treating, preventing, or protecting against the liver disease results in improvements in the liver function based upon changes in liver mass, liver lipids (e.g., triglyceride), expression of markers of liver fibrosis (e.g., Collal), liver inflammation (e.g., TNF alpha), and fatty acid oxidation gene expression (e.g., CPTla, Acoxl) liver imaging, blood metabolic panels, or blood liver protein levels.94. The use or method of embodiment 93, wherein the liver function is determined by serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), C reactive protein (CRP), triglyceride (TG), and HDL-C, LDL-C and total cholesterol.95. The use or method of embodiment 93, wherein the liver inflammation is determined by serum and hepatic expression of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin-1 (IL-1) levels.96. The use or method of any one of embodiments 4 to 95, wherein treating the liver disease comprises improvements in liver steatosis, liver inflammation (i.e., hepatitis), liver fibrosis, cirrhosis, or liver metabolism.97. The use or method of any one of embodiments 4 to 96, wherein treating the liver disease comprises an improvement in of serum levels of plasmalogens (e.g., lyso species), phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol), sphingolipids (e.g., ceramides, glycosphingolipids and sphingomyelins), glycerolipids (e.g., diacyl- and triacylglycerols), cholesterol, cholesterol esters, and free fatty acids.98. The use or method of embodiment 93, wherein the liver disease is measured by imaging to determine the extent of liver remodelling associated with steatosis, fibrosis, and cirrhosis.99. The use or method of any one of embodiments 1-98, wherein the treatment further comprises the use or administration of one or more alkylglycerols.100. The use or method of embodiment 99, wherein the composition further comprises the one or more alkylglycerols.Numbered Embodiments - Alzheimer's Disease1. A composition for use in treating a cognitive disease or disorder, such as Alzheimer’ s disease, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.2. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating a cognitive disease or disorder, such as Alzheimer’s disease.3. A method of treating a cognitive disease or disorder, such as Alzheimer’s disease, in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.4. The use or method of any one of embodiments 1 to 3, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.5. The use or method of any one of embodiments 1 to 4, wherein n is 2 or 3.6. The use or method of any one of embodiments 1 to 3, wherein Rx is methyl, and n is 3.7. The use or method of any one of embodiments 1 to 6, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.8. The use or method of embodiment 7, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted C14-24 acyl group.9. The use or method of any one of embodiments 1 to 8, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.10. The use or method of embodiment 9, wherein RA is an optionally substituted C14-18 alkyl group, an optionally substituted C14-18 alkenyl group, or an optionally substituted C14-18 acyl group.11. The use or method of embodiment 10, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.12. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkyl group.13. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkenyl group.14. The use or method of embodiment 11, wherein RA is an unsubstituted Ci6 alkyl group.15. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkyl group.16. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkenyl group.17. The use or method of any preceding embodiment, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).18. The use or method of any preceding embodiment, wherein the composition comprises a mixture of three compounds of Formula (I-A).19. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).20. The use or method of embodiment 19, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I- A3).21. The use or method of embodiment 19, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-Al), (I-A2), and (I-A3).22. The use or method of any one of embodiments 19 to 21, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).23. The use or method of any one of embodiments 17 to 19, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of (I-Al), (I-A2), and (I- A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.24. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).25. The use or method of embodiment 24, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).26. The use or method of embodiment 24, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).27. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I-A3).28. The use or method of embodiment 27, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).29. The use or method of embodiment 28, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I-A3).30. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I- A3).31. The use or method of embodiment 30, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).32. The use or method of embodiment 31, wherein the mixture has a molar ratio of from 0.72: 1 of (I-Al) to (I-A3).33. The use or method of embodiment 22, wherein the mixture has a molar percentage of (I- Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.34. The use or method of embodiment 33, wherein the mixture has a molar percentage of (I- Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I-A3) of 32.1%.35. The use or method of embodiment 33, wherein the mixture has a molar ratio of (I-A1):(I- A2):(I-A3) of 1 : 1.7: 1.4.36. The use or method of embodiment 23, wherein the mixture of at least two compounds is a 50:50 mixture.37. The use or method of embodiment 24, wherein the mixture of (I-Al), (I- A2) and (I-A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18:1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18:1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; orLPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.38. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-Al).39. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A2).40. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A3).41. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).42. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-A4), (I-A5), or (I-A6).43. The use or method of embodiment 42, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-A4), (I-A5), and (I-A6).44. The use or method of embodiment 42 or embodiment 34, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6).45. The use or method of embodiment 44, wherein the at least one compound is selected from a compound of Formula (I-A4), (I-A5) or (I-A6).46. The use or method of embodiment 42, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6), wherein said mixture of (I-A4), (I-A5), and (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.47. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 1.2:1 to 2.5:1 of (I-A5) to (I-A4).48. The use or method of embodiment 47, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A5) to (I-A4).49. The use or method of embodiment 48, wherein the mixture has a molar ratio of 1.7: 1 of (I-A5) to (I-A4).50. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A5) to (I-A6).51. The use or method of embodiment 50, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A5) to (I-A6).52. The use or method of embodiment 51, wherein the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6).53. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-A4) to (I-A6).54. The use or method of embodiment 53, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-A4) to (I-A6).55. The use or method of embodiment 54, wherein the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6).56. The use or method of embodiment 44, wherein the mixture has a molar percentage of (I- A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 26.8% to 37.4%.57. The use or method of embodiment 56, wherein the mixture has a molar percentage of (I- A4) of 24.8%, a molar percentage of (I-A5) of 42.4%, and a molar percentage of (I-A6) of 32.8%.58. The use or method of embodiment 56, wherein the mixture has a molar ratio of (I-A4):(I- A5):(I-A6) of 1 : 1.7: 1.3.59. The use or method of embodiment 46, wherein the mixture of the at least two compounds is a 50:50 mixture.60. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) is selected from:LPE(O-16:0) 26.8% + LPE(O-18:0) 46.1% + LPE(O-18: 1) 27.1%;LPE(O-16:0) 46% + LPE(O-18:0) 21% + LPE(O-18: 1) 33%;LPE(O-16:0) 42% + LPE(O-18:0) 51% + LPE(O-18: 1) 7%;LPE(O-16:0) 62% + LPE(O-18:0) 23.9% + LPE(O-18:1) 14.1%;LPE(O-16:0) 19.8% + LPE(O-18:0) 66% + LPE(O-18:1) 14.2%;LPE(O-16:0) 32.5% + LPE(O-18:0) 39.6% + LPE(O-18:1) 27.9%; orLPE(O-16:0) 34.1% + LPE(O-18:0) 41.5% + LPE(O-18:1) 24.4%.61. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A4).62. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A5).63. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A6).64. The use or method of any one of embodiments 1 to 63, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 4000 mg per day.65. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 2000 mg per day.66. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 1600 mg per day.67. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 400 mg, 800 mg, or 1600 mg per day.68. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 200 mg per day.69. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 100 mg per day.70. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 25 mg, 50 mg, or 100 mg per day.71. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 30 mg, 100 mg, or 300 mg per day.72. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical composition.73. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical formulation.74. The use or method of any one of embodiments 1-71, wherein the composition is a food.I l l75. The use or method of any one of embodiments 1-71, wherein the composition is a dietary supplement.76. The use or method of any one of embodiments 1-71, wherein the composition is a medicinal food.77. The use or method of any one of embodiments 1-76, wherein the composition is suitable for oral administration.78. The use or method of embodiment 77, wherein the oral administration form is a tablet, a capsule, a solution, a mouthwash, a suspension, a powder, a gum, a confectionary, a lozenge, a sublingual delivery system, or a rapid-melt formulation.79. The use or method of any one of embodiments 1-78, wherein the composition comprises at least one of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an antioxidant, an antifoaming agent, or a diluent.80. The use or method of embodiment 79, wherein the composition comprises at least one solubilizing agent.81. The use or method of embodiment 80, wherein the solubilizing agent is selected from the group consisting of carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, food grade solvents, phospholipids, DMSO, ethanol, ethyl acetate, and isopropanol.82. The use or method of any one of embodiments 1-81, wherein the cognitive disease or disorder is selected from the group consisting of Alzheimer’s disease, frontotemporal dementia, and schizophrenia83. The use or method of any one of embodiments 1-82, wherein the cognitive disease or disorder is Alzheimer’s disease.84. The use or method of any one of embodiments 1-83, wherein treating Alzheimer’s disease comprises reducing the symptoms associated with Alzheimer’s disease.85. The use or method of any one of embodiments 1-84, wherein treating Alzheimer’s disease comprises reducing a level of at least one biomarker in the subject.86. The use or method of embodiment 85, wherein the biomarkers are selected from blood biomarkers, cerebrospinal fluid biomarkers, MRI scans, PET scans, hippocampal volume, brain shrinkage, brain glucose metabolism.87. The use or method of embodiment 86, wherein the biomarkers are blood biomarkers or CSF biomarkers.88. The use or method of embodiment 87, wherein the blood biomarkers or the CSF biomarkers are selected from beta-amyloid 42, tau, and phospho-tau.89. The use or method of embodiment 84, wherein the symptoms associated with Alzheimer’s disease are determined using the Global Deterioration Scale.90. The use or method of embodiment 89, wherein the stage of symptoms is reduced on the Global Deterioration Scale.91. The use or method of any one of embodiments 83-90, wherein treating the Alzheimer’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Alzheimer’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined in any one of embodiments 1-81.92. The use or method of any one of embodiments 84-90, wherein reducing the symptoms associated with Alzheimer’s disease comprises the steps of:(a) determining the level of one or more biomarkers of Alzheimer’s disease from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined in any one of embodiments 1-81.93. The use or method of any one of embodiments 1-77, wherein the composition is a meal replacement therapy.94. The use or method of embodiment 93, wherein the meal replacement therapy is formulated for an adult subject.95. The use or method according to any one of embodiments 1-94, wherein the composition as defined in any of claims 1-82 additionally comprises one or more of an (N)-methyl-D-aspartate receptor antagonist, selective serotonin reuptake inhibitor or an acetylcholinesterase inhibitor.96. The use or method according to embodiment 95, wherein the acetylcholinesterase inhibitor is donepezil, rivastigmine, or galantamine.97. The use or method according to embodiment 95, wherein the (N)-methyl-D-aspartate receptor antagonist is memantine.98. The use or method according to embodiment 95, wherein the selective serotonin reuptake inhibitor is citalopram, escitalopram, paroxetine, or sertraline.99. The use or method of any one of embodiments 1-98, wherein the treatment further comprises the use or administration of one or more alkylglycerols.100. The use or method of embodiment 99, wherein the composition further comprises the one or more alkylglycerols.Numbered Embodiments - Peroxisomal disorders1. A composition for use in treating peroxisomal disorder and / or symptoms thereof, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.2. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating peroxisomal disorder and / or symptoms thereof.3. A method of treating peroxisomal disorder and / or symptoms thereof in a subject in need thereof, comprising administering to the subject an effective amount of a compositioncomprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.4. The use or method of any one of embodiments 1 to 3, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.5. The use or method of any one of embodiments 1 to 4, wherein n is 2 or 3.6. The use or method of any one of embodiments 1 to 3, wherein Rx is methyl, and n is 3.7. The use or method of any one of embodiments 1 to 6, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.8. The use or method of embodiment 7, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted C14-24 acyl group.9. The use or method of any one of embodiments 1 to 8, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.10. The use or method of embodiment 9, wherein RA is an optionally substituted C14-18 alkyl group, an optionally substituted C14-18 alkenyl group, or an optionally substituted C14-18 acyl group.11. The use or method of embodiment 10, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.12. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkyl group.13. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkenyl group.14. The use or method of embodiment 11, wherein RA is an unsubstituted Ci6 alkyl group.15. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkyl group.16. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkenyl group.17. The use or method of any preceding embodiment, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).18. The use or method of any preceding embodiment, wherein the composition comprises a mixture of three compounds of Formula (I-A).19. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).20. The use or method of embodiment 19, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I- A3).21. The use or method of embodiment 19, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-Al), (I-A2), and (I-A3).22. The use or method of any one of embodiments 19 to 21, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).23. The use or method of any one of embodiments 17 to 19, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of (I-Al), (I-A2), and (I- A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.24. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).25. The use or method of embodiment 24, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).26. The use or method of embodiment 24, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).27. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I-A3).28. The use or method of embodiment 27, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).29. The use or method of embodiment 28, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I-A3).30. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I- A3).31. The use or method of embodiment 30, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).32. The use or method of embodiment 31, wherein the mixture has a molar ratio of from 0.72: 1 of (I-Al) to (I-A3).33. The use or method of embodiment 22, wherein the mixture has a molar percentage of (I- Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.34. The use or method of embodiment 33, wherein the mixture has a molar percentage of (I- Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I-A3) of 32.1%.35. The use or method of embodiment 33, wherein the mixture has a molar ratio of (I-A1):(I- A2):(I-A3) of 1:1.7: 1.4.36. The use or method of embodiment 23, wherein the mixture of at least two compounds is a 50:50 mixture.37. The use or method of embodiment 24, wherein the mixture of (I-Al), (I- A2) and (I-A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18:1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18:1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; orLPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.38. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-Al).39. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A2).40. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A3).41. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).42. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-A4), (I-A5), or (I-A6).43. The use or method of embodiment 42, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-A4), (I-A5), and (I-A6).44. The use or method of embodiment 42 or embodiment 34, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6).45. The use or method of embodiment 44, wherein the at least one compound is selected from a compound of Formula (I-A4), (I-A5) or (I-A6).46. The use or method of embodiment 42, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6), wherein said mixture of (I-A4), (I-A5), and (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.47. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A5) to (I-A4).48. The use or method of embodiment 47, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A5) to (I-A4).49. The use or method of embodiment 48, wherein the mixture has a molar ratio of 1.7: 1 of (I-A5) to (I-A4).50. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A5) to (I-A6).51. The use or method of embodiment 50, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A5) to (I-A6).52. The use or method of embodiment 51, wherein the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6).53. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-A4) to (I-A6).54. The use or method of embodiment 53, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-A4) to (I-A6).55. The use or method of embodiment 54, wherein the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6).56. The use or method of embodiment 44, wherein the mixture has a molar percentage of (I- A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 26.8% to 37.4%.57. The use or method of embodiment 56, wherein the mixture has a molar percentage of (I- A4) of 24.8%, a molar percentage of (I-A5) of 42.4%, and a molar percentage of (I-A6) of 32.8%.58. The use or method of embodiment 56, wherein the mixture has a molar ratio of (I-A4):(I- A5):(I-A6) of 1 : 1.7: 1.3.59. The use or method of embodiment 46, wherein the mixture of the at least two compounds is a 50:50 mixture.60. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) is selected from:LPE(O-16:0) 26.8% + LPE(O-18:0) 46.1% + LPE(O-18: 1) 27.1%;LPE(O-16:0) 46% + LPE(O-18:0) 21% + LPE(O-18: 1) 33%;LPE(O-16:0) 42% + LPE(O-18:0) 51% + LPE(O-18: 1) 7%;LPE(O-16:0) 62% + LPE(O-18:0) 23.9% + LPE(O-18:1) 14.1%;LPE(O-16:0) 19.8% + LPE(O-18:0) 66% + LPE(O-18:1) 14.2%;LPE(O-16:0) 32.5% + LPE(O-18:0) 39.6% + LPE(O-18:1) 27.9%; orLPE(O-16:0) 34.1% + LPE(O-18:0) 41.5% + LPE(O-18:1) 24.4%.61. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A4).62. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A5).63. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A6).64. The use or method of any one of embodiments 1 to 63, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 4000 mg per day.65. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 0.1 to 2000 mg per day.66. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 1600 mg per day.67. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 400 mg, 800 mg, or 1600 mg per day.68. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 200 mg per day.69. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 100 mg per day.70. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 25 mg, 50 mg, or 100 mg per day.71. The use or method of embodiment 64, wherein the compound of Formula (I-A) is administered in a dose of 30 mg, 100 mg, or 300 mg per day.72. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical composition.73. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical formulation.74. The use or method of any one of embodiments 1-71, wherein the composition is a food.75. The use or method of any one of embodiments 1-71, wherein the composition is food supplement.76. The use or method of any one of embodiments 1-71, wherein the composition is a medicinal food.77. The use or method of any one of embodiments 1-76, wherein the composition is suitable for oral administration.78. The use or method of embodiment 77, wherein the oral administration form is a tablet, a capsule, a solution, a mouthwash, a suspension, a powder, a gum, a confectionary, a lozenge, a sublingual delivery system, or a rapid-melt formulation.79. The use or method of any one of embodiments 1-78, wherein the composition comprises at least one of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an antioxidant, an antifoaming agent, or a diluent.80. The use or method of embodiment 79, wherein the composition comprises at least one solubilizing agent.81. The use or method of embodiment 80, wherein the solubilizing agent is selected from the group consisting of carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, food grade solvents, phospholipids, DMSO, ethanol, ethyl acetate, and isopropanol.82. The use or method of any one of embodiments 1-81, wherein treating a peroxisomal disorder and / or symptoms thereof comprises treating rhizomelic chondrodysplasia punctata, Zellweger spectrum disorders, Refsum Disease, X-Linked Adrenoleukodystrophy.83. The use or method of embodiment 82, wherein Zellweger spectrum disorder comprises Zellweger Syndrome, Neonatal Adrenoleukodystrophy, Refsum Disease and Infantile Refsum Disease.84. The use or method of embodiment 82 or embodiment 83, wherein treating a peroxisomal disorder and / or symptoms thereof comprises treating rhizomelic chondrodysplasia punctata, or Zellweger syndrome.85. The use or method of any one of embodiments 1-84, wherein treating a peroxisomal disorder and / or symptoms thereof comprises treating the symptoms associated with a peroxisomal disease.86. The use or method of embodiment 85, wherein treating the symptoms associated with a peroxisomal disorder comprises reducing the symptoms associated with a peroxisomal disorder.87. The use or method of any one of embodiments 1-86, wherein treating a peroxisomal disorder and / or symptoms thereof comprises reducing a level of at least one biomarker in the subject.88. The use or method of embodiment 87, wherein the biomarkers are selected from blood biomarkers, cerebrospinal fluid biomarkers, single photon emission computed tomography scan, MRI scan, CT scan.89. The use or method of embodiment 88, wherein the biomarkers are cortical and cerebellar migrational abnormalities, central white-matter demyelination, blood biomarkers or CSF biomarkers.90. The use or method of embodiment 89, wherein the blood biomarkers or the CSF biomarkers are very-long-chain fatty acids, phytanic acid, pipecolic acids, and deficient synthesis of plasmalogens, elevated protein levels.91. The use or method of embodiment 90, wherein reducing the level of the biomarker comprises one or more of reducing the levels of phytanic acid in the subject.92. The use or method of embodiment 85, wherein the symptoms associated with peroxisomal disorders are nerve damage, retinopathy, hearing loss, anosmia, spastic movements, and changes in the bone and skin, demyelination, seizures, hypotonia, enlarged liver, hepatic cysts, cataracts, hearing loss, bradykinesia, and weakness, numbness, and pain in the hands and feet.93. The use or method of embodiment 86, wherein reducing the symptoms comprises reducing seizure severity, reducing the frequency of seizure, slowing the progression of retinopathy, slowing the progression of hearing loss, slowing the progression of anosmia, reducing the frequency of spastic movements, slowing the progression of demyelation.94. The use or method of any one of embodiments 82-93, wherein treating peroxisomal disorder and / or symptoms comprises the steps of:(a) determining the level of one or more biomarkers of a peroxisomal disorder from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined in any one of embodiments 1-81.95. The use or method of any one of embodiments 84-94, wherein treating the symptoms associated with a peroxisomal disorder comprises the steps of:(a) determining the level of one or more biomarkers of a peroxisomal disorder from the patient;(b) comparing the level of the biomarker with a control level, wherein a positive determination is made if the level of biomarker in the biological sample is statistically significantly higher or lower than the control level; and(c) administering to the patient an effective amount of a composition as defined in any one of embodiments 1-81.96. The use or method of any one of embodiments 1-77, wherein the composition is a meal replacement therapy.97. The use or method of embodiment 96, wherein the meal replacement therapy is formulated for an adult subject.98. The use or method of embodiment 96, wherein the meal replacement therapy is formulated for an infant subject.99. The use or method according to any one of embodiments 1-98, wherein the composition as defined in any of embodiments 1-81 additionally comprises cholic acid.100. The use or method of any one of embodiments 1-99, wherein the treatment further comprises the use or administration of one or more alkylglycerols.101. The use or method of embodiment 100, wherein the composition further comprises the one or more alkylglycerols.Numbered Embodiments - Neonatal1. A composition for use in increasing the levels of plasmalogens in an infant, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.2. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a composition for use in increasing the levels of plasmalogens in an infant.3. A method of increasing the levels of plasmalogens in an infant, comprising adding an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof to a nutritional formulation for the infant.4. The use or method of any one of embodiments 1 to 3, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.5. The use or method of any one of embodiments 1 to 4, wherein n is 2 or 3.6. The use or method of any one of embodiments 1 to 3, wherein Rx is methyl, and n is 3.7. The use or method of any one of embodiments 1 to 6, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.8. The use or method of embodiment 7, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted C14-24 acyl group.9. The use or method of any one of embodiments 1 to 8, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.10. The use or method of embodiment 9, wherein RA is an optionally substituted C14-18 alkyl group, an optionally substituted C14-18 alkenyl group, or an optionally substituted C14-18 acyl group.11. The use or method of embodiment 10, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.12. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkyl group.13. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkenyl group.14. The use or method of embodiment 11, wherein RA is an unsubstituted Ci6 alkyl group.15. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkyl group.16. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkenyl group.17. The use or method of any preceding embodiment, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).18. The use or method of any preceding embodiment, wherein the composition comprises a mixture of three compounds of Formula (I-A).19. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).20. The use or method of embodiment 19, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I- A3).21. The use or method of embodiment 19, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-Al), (I-A2), and (I-A3).22. The use or method of any one of embodiments 19 to 21, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).23. The use or method of any one of embodiments 17 to 19, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of (I-Al), (I-A2), and (I- A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.24. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).25. The use or method of embodiment 24, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).26. The use or method of embodiment 24, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).27. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I-A3).28. The use or method of embodiment 27, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).29. The use or method of embodiment 28, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I-A3).30. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I- A3).31. The use or method of embodiment 30, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).32. The use or method of embodiment 31, wherein the mixture has a molar ratio of from 0.72: 1 of (I-Al) to (I-A3).33. The use or method of embodiment 22, wherein the mixture has a molar percentage of (I- Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.34. The use or method of embodiment 33, wherein the mixture has a molar percentage of (I- Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I-A3) of 32.1%.35. The use or method of embodiment 33, wherein the mixture has a molar ratio of (I-A1):(I- A2):(I-A3) of 1 : 1.7: 1.4.36. The use or method of embodiment 23, wherein the mixture of at least two compounds is a50:50 mixture.37. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18: 1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18: 1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; orLPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.38. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-Al).39. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A2).40. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A3).41. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).42. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-A4), (I-A5), or (I-A6).43. The use or method of embodiment 42, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-A4), (I-A5), and (I-A6).44. The use or method of embodiment 42 or embodiment 34, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6).45. The use or method of embodiment 44, wherein the at least one compound is selected from a compound of Formula (I-A4), (I-A5) or (I-A6).46. The use or method of embodiment 42, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6), wherein said mixture of (I-A4), (I-A5), and (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.47. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 1.2:1 to 2.5:1 of (I-A5) to (I-A4).48. The use or method of embodiment 47, wherein the mixture has a molar ratio of from 1.5:1 to 2.1:1 of (I-A5) to (I-A4).49. The use or method of embodiment 48, wherein the mixture has a molar ratio of 1.7: 1 of (I-A5) to (I-A4).50. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.9:1 to 1.7:1 of (I-A5) to (I-A6).51. The use or method of embodiment 50, wherein the mixture has a molar ratio of from 1 : 1 to 1.5:1 of (I-A5) to (I-A6).52. The use or method of embodiment 51, wherein the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6).53. The use or method of embodiment 42, wherein the mixture has a molar ratio of from 0.5:1 to 1:1 of (I-A4) to (I-A6).54. The use or method of embodiment 53, wherein the mixture has a molar ratio of from 0.6:1 to 0.9:1 of (I-A4) to (I-A6).55. The use or method of embodiment 54, wherein the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6).56. The use or method of embodiment 44, wherein the mixture has a molar percentage of (I- A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 26.8% to 37.4%.57. The use or method of embodiment 56, wherein the mixture has a molar percentage of (I- A4) of 24.8%, a molar percentage of (I-A5) of 42.4%, and a molar percentage of (I-A6) of 32.8%.58. The use or method of embodiment 56, wherein the mixture has a molar ratio of (I-A4):(I- A5):(I-A6) of 1:1.7: 1.3.59. The use or method of embodiment 46, wherein the mixture of the at least two compounds is a 50:50 mixture.60. The use or method of embodiment 47, wherein the mixture of (I-A4), (I-A5) and (I-A6) is selected from:LPE(O-16:0) 26.8% + LPE(O-18:0) 46.1% + LPE(O-18:1) 27.1%;LPE(O-16:0) 46% + LPE(O-18:0) 21% + LPE(O-18:1) 33%;LPE(O-16:0) 42% + LPE(O-18:0) 51% + LPE(O-18:1) 7%;LPE(O-16:0) 62% + LPE(O-18:0) 23.9% + LPE(O-18:1) 14.1%;LPE(O-16:0) 19.8% + LPE(O-18:0) 66% + LPE(O-18:1) 14.2%;LPE(O-16:0) 32.5% + LPE(O-18:0) 39.6% + LPE(O-18:1) 27.9%; orLPE(O-16:0) 34.1% + LPE(O-18:0) 41.5% + LPE(O-18:1) 24.4%.61. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A4).62. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A5).63. The use or method of embodiment 44, wherein the mixture of (I-A4), (I-A5) and (I-A6) comprises 90% w / v (I-A6).64. The use or method of any one of embodiments 1 to 63, wherein the compound comprises from 35-442 pM of the mixture of (I-Al), (I-A2), and (I-A3).65. The use or method of any one of embodiments 1 to 64, wherein the compound comprises from 35-247 pM of the mixture of (I-A4), (I-A5), and (I-A6).66. The use or method of any one of embodiments 1 to 65, wherein the composition comprises one or more alkylglycerols (AKG).67. The use or method of embodiment 66, wherein the composition comprises from 110-805 pM AKG.68. The use or method of any one of embodiments 1 to 63, wherein the compound comprises: (i) a mixture of (I-Al), (I-A2), and (I-A3), or (ii) a mixture of (I-A4), (I-A5), and (I-A6); and one or more alkylglycerols (AKG).69. The use or method of any one of embodiments 1 to 63, wherein the compound comprises: (i) from 35-442 pM of the mixture of (I-Al), (I-A2), and (I- A3), or (ii) from 35-247 pM of the mixture of (I-A4), (I-A5), and (I-A6); and from 110-805 pM of one or more alkylglycerols (AKG).70. The use or method of any one of embodiments 1 to 63, wherein the compound comprises: LPC(O) or LPE(O); and one or more alkylglycerols (AKG).71. The use or method of any one of embodiments 1 to 63, wherein the compound comprises: from 35-442 pM of LPC(O) or from 35-247 pM of LPE(O); and from 110-805 pM of one or more alkylglycerols (AKG).72. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical composition.73. The use or method of any one of embodiments 1-71, wherein the composition is a pharmaceutical formulation.74. The use or method of any one of embodiments 1-71, wherein the composition is a food.75. The use or method of any one of embodiments 1-71, wherein the composition is dietary supplement.76. The use or method of any one of embodiments 1-71, wherein the composition is a medicinal food.77. The use or method of any one of embodiments 1-76, wherein the composition is suitable for oral administration.78. The use or method of embodiment 77, wherein the oral administration form is a tablet, a capsule, a solution, a mouthwash, a suspension, a powder, a gum, a confectionary, a lozenge, a sublingual delivery system, or a rapid-melt formulation.79. The use or method of any one of embodiments 1-76, wherein the composition is a nutritional formulation for infants.80. The use or method of any one of embodiments 1-76, wherein the composition is a dietary supplement for a breast-feeding mother of the infant.81. The use or method of any one of embodiments 1-76, wherein the composition is an infant formula.82. The use or method of any one of embodiments 1-81, wherein the composition comprises at least one of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an antioxidant, an antifoaming agent, or a diluent.83. The use or method of embodiment 82, wherein the composition comprises at least one solubilizing agent.84. The use or method of embodiment 83, wherein the solubilizing agent is selected from the group consisting of carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, food grade solvents, phospholipids, DMSO, ethanol, ethyl acetate, and isopropanol.85. The use or method of any one of embodiments 1-84, wherein administration of the composition improves the immunity of the infant.86. The use or method of any one of embodiments 1-84, wherein administration of the composition reduces inflammation in the infant.87. The use or method of any one of embodiments 1-84, wherein administration of the composition reduces the number of infections in the infant.88. The use or method of any one of embodiments 1-84, wherein administration of the composition improves neurodevelopment in the infant.Numbered Embodiments - Cardiac1 . A composition for use in treating cardiovascular disease, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.2. Use of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating cardiovascular disease.3. A method of treating cardiovascular disease in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.4. The use or method of any one of embodiments 1 to 3, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.5. The use or method of any one of embodiments 1 to 4, wherein n is 2 or 3.6. The use or method of any one of embodiments 1 to 3, wherein Rx is methyl, and n is 3.7. The use or method of any one of embodiments 1 to 6, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.8. The use or method of embodiment 7, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted C14-24 acyl group.9. The use or method of any one of embodiments 1 to 8, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.10. The use or method of embodiment 9, wherein RA is an optionally substituted C14-18 alkyl group, an optionally substituted C14-18 alkenyl group, or an optionally substituted C14-18 acyl group.11. The use or method of embodiment 10, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.12. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkyl group.13. The use or method of embodiment 11, wherein RA is an optionally substituted C16-18 alkenyl group.14. The use or method of embodiment 11, wherein RA is an unsubstituted Ci6 alkyl group.15. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkyl group.16. The use or method of embodiment 11, wherein RA is an unsubstituted Cis alkenyl group.17. The use or method of any preceding embodiment, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).18. The use or method of any preceding embodiment, wherein the composition comprises a mixture of three compounds of Formula (I-A).19. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).20. The use or method of embodiment 19, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I- A3).21. The use or method of embodiment 19, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-Al), (I-A2), and (I-A3).22. The use or method of any one of embodiments 19 to 21, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).23. The use or method of any one of embodiments 17 to 19, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of (I-Al), (I-A2), and (I- A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.24. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).25. The use or method of embodiment 24, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).26. The use or method of embodiment 24, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).27. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I-A3).28. The use or method of embodiment 27, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).29. The use or method of embodiment 28, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I-A3).30. The use or method of embodiment 18, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I- A3).31. The use or method of embodiment 30, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).32. The use or method of embodiment 31, wherein the mixture has a molar ratio of from 0.72:1 of (I-Al) to (I-A3).33. The use or method of embodiment 22, wherein the mixture has a molar percentage of (I- Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.34. The use or method of embodiment 33, wherein the mixture has a molar percentage of (I- Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I-A3) of 32.1%.35. The use or method of embodiment 33, wherein the mixture has a molar ratio of (I-A1):(I- A2):(I-A3) of 1:1.7: 1.4.36. The use or method of embodiment 23, wherein the mixture of at least two compounds is a 50:50 mixture.37. The use or method of embodiment 24, wherein the mixture of (I-Al), (I- A2) and (I-A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18:1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18:1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; orLPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.38. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-Al).39. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A2).40. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) comprises 90% w / v (I-A3).41. The use or method of embodiment 24, wherein the mixture of (I-Al), (I-A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).42. The use or method of any one of embodiments 1 to 3, wherein the compound of Formula (I-A) is of the structure (I-A4), (I-A5), or (I-A6).43...

Claims

CLAIMS1. A composition for use in the treatment, prevention and / or amelioration of a plasmalogen-associated disorder in a subject, wherein the composition comprises at least one compound of formula (I-A),I-A) , wherein RA is a hydrocarbon chain, and the Rxgroups are each independently selected from the group consisting of: hydrogen, and Ci-3alkyl.

2. The composition for use of claim 1, wherein the plasmalogen-associated disorder is a plasmalogen-deficient disorder.

3. The composition for use of any preceding claims, wherein the plasmalogen-associated disorder is selected from the group consisting of: a metabolic disorder, a neurological disorder, an inflammatory disorder, a cardiovascular disorder, a peroxisomal disorder, and a neonatal disorder.

4. The composition for use of any preceding claims, wherein the plasmalogen-associated disorder is a metabolic disorder.

5. The composition for use according to claim 4, wherein the metabolic disorder is selected from the group consisting of: a liver disease, diabetes, obesity, a lipid disorder, metabolic syndrome, a cardiovascular disorder, and a mitochondrial disorder.

6. The composition for use according to any of claims 4-5, wherein the metabolic disorder is a liver disease, such as a liver disease selected from the group consisting of: nonalcoholic fatty liver disease, non-alcoholic steatohepatitis, liver steatosis, hepatitis, liver fibrosis, cirrhosis, and liver cancer.

7. The composition for use according to any of claims 4-6, wherein the metabolic disorder is obesity, diabetes, such as Type-II-diabetes, and / or dyslipidemia.

8. The composition for use according to any of claims 4-7, wherein the composition comprises a lysoalkylphosphatidylethanolamine (LPE(O)).

9. The composition for use according to any of claims 4-8, wherein the composition comprises Cl 8.0 LPE(O), and / or Cl 6.0 LPE(O).

10. The composition for use according to any of claims 4-9, wherein the comprises a mixture of 2 or more of C18.0, C16.0, and C18.1 LPE(O)s.

11. The composition for use according to any of claims 4-10, wherein the comprises a mixture of about 55% Cl 6.0 LPE(O) and about 45% Cl 8.0 LPE(O).

12. The composition for use according to any of claims 4-10, wherein the comprises a mixture of about 50% Cl 6.0 LPE(O) and about 50% Cl 8.0 LPE(O).

13. The composition for use according to any of claims 4-10, wherein the comprises 16:0, 18:0, and 18: 1 at a 2:2: 1 ratio.

14. The composition for use according to any of claims 4-10, wherein the composition comprises 16:0, 18:0, and 18: 1 at a 40:30:30 ratio.

15. The composition for use according to any of claims 4-14, wherein the composition comprises a lysoalkylphosphatidylcholine, LPC(O).

16. The composition for use according to any of claims 4-15, wherein the composition additionally comprises AKGs.

17. The composition for use according to any of claims 4-16, wherein the composition additionally comprises omega-3 fatty acids.

18. The composition for use according to claims 17, wherein the omega-3 fatty acids are selected from the group consisting of: DHA, EP A, and a combination thereof.

19. The composition for use according to claim 18, wherein a dose of 0.25-6.8 grams / day of the omega 3 fatty acids is administered to the subject.

20. The composition for use according to any of claims 4-19, wherein composition is administered in a daily dosage of about from 1 to 100 mg / kg / day to the subject with respect to LPX(O).

21. The composition for use according to any of claims 4-20, wherein a GLP-1 receptor agonist is co-administered to the subject, prior to, concomitantly with, or subsequent to the composition, optionally wherein the GLP-1 receptor agonist is semaglutide.

22. The composition for use according to any of claims 1-3, wherein the plasmalogen- associated disorder is a neurological disorder.

23. The composition for use according to claim 22, wherein the neurological disorder is selected from the group consisting of: a neuronal maturation disorder including a peroxisomal disorder, an infant brain development disorder, Zellweger spectrum disorder, rhizomelic chondrodysplasia punctata, and autism spectrum disorder; a neuronal regeneration disorder including multiple sclerosis (MS), and peripheral neuropathy; a cognitive disorder, including Alzheimer’s disease, mild cognitive impairment, vascular dementia, and age-related cognitive decline; and a movement disorder, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

24. The composition for use according to claim 22, wherein the neurological disorder is selected from the group consisting of: Alzheimer's disease (AD), Parkinson’s disease (PD), Multiple sclerosis (MS), autism spectrum disorder, and amyotrophic lateral sclerosis (ALS).

25. The composition for use according to any of claims 22-24, wherein the composition is administered to the subject for treatment of a movement disorder, for example Parkinson’s disease or Multiple Sclerosis (MS), wherein the composition comprises at least one LPE(O).

26. The composition for use according to any of claims 22-24, wherein the composition is administered for treatment of a cognitive disorder, wherein the cognitive disorder is Alzheimer’s Disease, dementia, Lewy-body dementia, or Parkinson’s disease.

27. The composition for use according to any of claims 22-26, wherein the composition is administered in a daily dosage to the subject of from 1 mg / kg to 100 mg / kg / day.

28. The composition for use according to any of claims 22-27, wherein the composition further comprises one or more omega-3 fatty acids, such as DHA, for example wherein the one or more fatty acids are administered to the subject at a dose of from 1 to 10 mg / kg / day.

29. The composition for use according to any of claims 22-28, wherein the composition comprises PE(O) at a dosage of from 2 to 35 mg / kg / day.

30. The composition for use according to any of claims 22-29, wherein the composition further comprises an omega-6 fatty acid, such as ARA, optionally at a dose of about from 80 to 240 mg / day.

31. The composition for use according to any of claims 22-25, wherein administration of the composition to the subject delays the onset of MS symptoms and / or improves recovery time from the MS symptoms.

32. The composition for use according to any of claims 22-25, or 31, wherein the composition is administered to the subject for treatment of MS, wherein the composition comprises one or more LPE(O)s and is administered to the subject in combination with fmgolimod, optionally wherein fmgolimod is administered in a dose of about from 0.3 mg / kg / day to 10 mg / kg / day.

33. The composition for use according to any of claims 22-25, or 31-32, wherein the composition comprises an effective amount of at least one compound of Formula (I- A) of at least about 19 mg / kg / day.

34. The composition for use according to any of claims 22-25, or 31-33, wherein the composition comprises about a 50:50 mixture of LPE(O) C16.0:C18.0.

35. The composition for use according to any of claims 22-25, or 31-33, wherein the composition comprises about a 2:2: 1 mixture of C16.0, C18.0, and C18.1 LPE(O)s.

36. The composition for use according to any of claims 22-25, or 31-33, wherein the composition comprises about a 40:30:30 mixture of C16.0 / C18.0 / C18.1 LPE(O).

37. The composition for use according to any of claims 1-3, wherein the plasmalogen- associated disorder is an inflammatory disorder.

38. The composition for use according to claim 37, wherein the inflammatory disorder is selected from the group consisting of: an autoimmune disease, such as rheumatoid arthritis (RA), lupus, psoriasis, inflammatory bowel disease (IBD), multiple sclerosis (MS), and ankylosing spondylitis; a cardiovascular disease; a gastrointestinal disorder, such as inflammatory bowel disease (IBD), Crohn’s disease, and ulcerative colitis (UC); type-2-diabetes; a neurodegenerative disease; and bronchopulmonary dysplasia (BPD).

39. The composition for use according to claim 37, wherein the inflammatory disorder is rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), Psoriasis, Asthma, and Chronic Obstructive Pulmonary Disease (COPD).

40. The composition for use according to any of claims 37-39, wherein the composition is administered to the subject for treatment of a cardiovascular disease, and wherein thecomposition comprises about a 40:30:30 mixture of C16.0 / C18.0 / C18.1 LPE(O)s and / or AKGs.

41. The composition for use according to any of claims 37-39, wherein the composition is administered for treatment of MS, and wherein the composition comprises 55% LPE(O) C16:0 and 45% LPE(O) C18:0.

42. The composition for use according to any of claims 37-39, wherein the composition is administered to the subject in a daily dosage of from 1 mg / kg to 100 mg / kg / day.

43. The composition for use according to any of claims 37-39, wherein the inflammatory disorder is rheumatoid arthritis.

44. The composition for use according to any of claims 37-39, wherein the composition additionally comprises one or more omega-3 fatty acids, such as DHA, and / or further comprises EPA at a dose of from 250 mg to 3 g / day.

45. The composition for use according to any of claims 1-3, wherein the plasmalogen- associated disorder is a cardiovascular disorder.

46. The composition for use according to claim 45, wherein the cardiovascular disorder is atherosclerosis, coronary artery disease, heart failure, hypertension, arrhythmias, and peripheral artery disease.

47. The composition for use according to any of claims 45-46, wherein the cardiovascular disorder is acute or chronic.

48. The composition for use according to any of claims 45-47, wherein the composition is administered to a subject for treatment of ischemia reperfusion injury.

49. The composition for use according to any of claims 45-48, wherein the composition is administered to a subject to prevent ischemia reperfusion injury or to decrease the pathological effects resulting from ischemia reperfusion injury.

50. The composition for use according to any of claims 45-49, wherein the composition is administered to a subject to protect against heart failure and ischemia reperfusion injury.

51. The composition for use according to any of claims 45-50, wherein the composition is administered to a subject immediately, such as from 5 seconds to 12 hours following onset of a myocardial infarction, such as an acute myocardial infarction.

52. The composition for use according to any of claims 45-51, wherein the composition comprises a mixture of about 40% LPE(O-16:0), about 30% LPE(O-18:0), and about 30% LPE(O-18: 1), and optionally one or more AKGs.

53. The composition for use according to any of claims 45-52, wherein the composition is administered to the subject in a daily dosage of from 1 mg / kg / day to 100 mg / kg / day.

54. The composition for use according to any of claims 45-53, wherein the composition further comprises one or more AKGs, for example at a dosage of from 1.5 to 50 mg / kg / day.

55. The composition for use according to any of claims 45-54, wherein the treatment further comprises administration of an omega-3 fatty acid, such as ALA, DHA, or EPA.

56. The composition for use according to claim 3, wherein the plasmalogen-associated disorder is a peroxisomal disorder, for example Zellweger spectrum disorder.

57. The composition for use according to claim 56, wherein administration of the composition prevents, treats and / or alleviates a peroxisomal disorder, prevents and / or ameliorates a neurodevelopment disorder, and / or assists in development of infant immune system.

58. The composition for use according to any of claims 56-57, wherein the composition is administered to the subject and comprises LPC(O) and / or LPE(O) with alkyl chains of 16 or 18 in length.

59. The composition for use according to claim 58, wherein the LPE(O) and / or LPC(O) is a mixture of about 55:45 C16.0 to C18.0 LPE(O).

60. The composition for use according to claim 58, wherein the LPE(O) and / or LPC(O) is a 50:50 mixture of C16.0 to C18.0 LPE(O).

61. The composition for use according to claim 58, wherein the LPE(O) or LPC(O) is a 2:2: 1 mixture of 16.0, 18.0, 18.1 LPE(O) or LPC(O).

62. The composition for use according to any of claims 56-61, wherein the composition is administered for treatment of Rhizomelic chondrodysplasia punctata or Zellweger Syndrome, wherein the subject is an infant or toddler, for example a toddler or infant characterized by an inability to synthesize a sufficient amount of plasmalogens in their peroxisomes.

63. The composition for use according to any of claims 56-62, wherein the composition is administered in a daily dosage of from 0.2 mg / kg / day to 25 mg / kg / day, or from 0.1 mg to 4000 mg LPC(O) equivalents per day.

64. The composition for use according to any of claims 56-63, wherein the composition is administered to the subject for treatment and / or prevention of neurodevelopment disorders, and development of infant immune systems, wherein the composition comprises LPC(O) and / or LPE(O) with alkyl chains of 16 or 18 in length.

65. The composition for use according to any of claims 56-64, wherein the composition further comprises one or more AKGs.

66. The composition for use according to any of claims 56-65, wherein the composition further comprises one or more polyunsaturated fatty acids, such as EP A, ARA and / or DHA, for example in a dosage of 250-500 mg / day fatty acids or from 10 mg / kg / day to 12 mg / kg / day.

67. Use of a composition for raising the level of one or more plasmalogens, alkylphosphatidylcholine PE(C), and / or alkylphosphatidylethanolamine PE(O) in a subject, comprising administering the composition to the subject, the composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.

68. The use of claim 67, wherein the one or more plasmalogens are independently selected from the group consisting of: PE(P), and PC(P).

69. The use of claim 67, wherein the use comprises raising the level of PE(O) and / or PC(O).

70. The use of any of claims 67-69, wherein the level of one or more plasmalogens, and / or phospholipids, such as alkylphosphatidylcholine PC(O), and / or alkylphosphatidylethanolamine PE(O) in the subject is increased in circulation, such as in blood plasma, and / or in a target tissue.

71. The use of claim 70, wherein the target tissue is selected from the group consisting of: brain tissue, neurological tissue, liver tissue, heart tissue, kidney tissue, pancreas tissue, colon tissue, intestines tissue, within cells peroxisomes and mitochondria.

72. A composition for use in increasing the levels of plasmalogens in an infant, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.

73. A composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof in the manufacture of a composition for use in increasing the levels of plasmalogens in an infant.

74. A method of increasing the levels of plasmalogens in an infant or a lactating woman, comprising adding an effective amount of a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof to a nutritional formulation for the infant and / or lactating woman.

75. The composition for use or method according to any of claims 72-74, wherein administration of the composition improves the immunity of the infant.

76. The composition for use or method according to any of claims 72-75, wherein administration of the composition reduces inflammation in the infant.

77. The composition for use or method according to any of claims 72-76, wherein administration of the composition reduces the number of infections in the infant.

78. The composition for use or method according to any of claims 72-77, wherein administration of the composition improves neurodevelopment in the infant.

79. The composition for use or method according to any of claims 72-78, wherein the composition is administered in the form of an infant formula, such as a fortified infant formula.

80. A method of increasing levels of PE(O)s and / or PC(O)s in a subject, comprising administering a composition comprising at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof, to the subject.

81. The method of claim 80, wherein the levels of PE(O)s and / or PC(O)s are increased in circulation and / or tissue.

82. A composition for use in preventing weight gain and / or promoting weight loss, wherein the composition comprises at least one compound of Formula (I-A) or a pharmaceutically acceptable salt thereof.

83. Use of a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for preventing weight gain and / or promoting weight loss.

84. A method of preventing weight gain and / or promoting weight loss in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.

85. A composition for use in treating, preventing, or protecting against liver disease, wherein the composition comprises at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.

86. Use of a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating, preventing, or protecting against liver disease.

87. A method of treating, preventing, or protecting against liver disease in a subject in need thereof, comprising administering to the subject an effective amount of a composition comprising at least one compound of Formula (I- A) or a pharmaceutically acceptable salt thereof.

88. The composition for use, use or method of any one of claims 1 to 87, wherein each Rx is independently selected from hydrogen or C1-3 alkyl.

89. The composition for use, use or method of any one of claims 1 to 88, wherein n is 2 or 3.

90. The composition for use, use or method of any one of claims 1 to 87, wherein Rx is methyl, and n is 3.

91. The composition for use, use or method of any one of claims 1 to 90, wherein RA is an optionally substituted hydrocarbon chain containing from 14 to 24 carbon atoms.

92. The composition for use, use or method of claim 91, wherein RA is an optionally substituted C14-24 alkyl group, an optionally substituted C14-24 alkenyl group, or an optionally substituted Ci4-24 acyl group.

93. The composition for use, use or method of any one of claims 1 to 92, wherein RA is an optionally substituted hydrocarbon chain containing from 16 to 18 carbon atoms.

94. The composition for use, use or method of claim 93, wherein RA is an optionally substituted Cu-is alkyl group, an optionally substituted Cu-18 alkenyl group, or an optionally substituted C14-18 acyl group.

95. The composition for use, use or method of claim 94, wherein RA is an optionally substituted C16-18 alkyl group, an optionally substituted C16-18 alkenyl group, or an optionally substituted C16-18 acyl group.

96. The composition for use, use or method of claim 95, wherein RA is an optionally substituted C16-18 alkyl group.

97. The composition for use, use or method of claim 95, wherein RA is an optionally substituted C16-18 alkenyl group.

98. The composition for use, use or method of claim 95, wherein RA is an unsubstituted Ci6 alkyl group.

99. The composition for use, use or method of claim 95, wherein RA is an unsubstituted Cis alkyl group.

100. The composition for use, use or method of claim 95, wherein RA is an unsubstituted Cis alkenyl group.

101. The composition for use, use or method of any preceding claim, wherein the composition comprises a mixture of at least two compounds of Formula (I-A).

102. The composition for use, use or method of any preceding claim, wherein the composition comprises a mixture of three compounds of Formula (I-A).

103. The composition for use, use or method of any one of claims 1 to 87, wherein the compound of Formula (I-A) is of the structure (I-Al), (I-A2), or (I-A3).

104. The composition for use, use or method of claim 103, wherein the at least one compound is selected from a compound of Formula (I-Al), (I-A2) or (I-A3).

105. The composition for use, use or method of claim 103, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I- Al), (I-A2), and (I-A3).

106. The composition for use, use or method of any one of claims 103 to 105, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3).

107. The composition for use, use or method of any one of claims lOlto 103, wherein the composition comprises a mixture of (I-Al), (I-A2), and (I-A3), wherein said mixture of(I-Al), (I-A2), and (I-A3) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.

108. The composition for use, use or method of claim 102, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A2) to (I-Al).

109. The composition for use, use or method of claim 108, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A2) to (I-Al).

110. The composition for use, use or method of claim 108, wherein the mixture has a molar ratio of 1.7: 1 of (I-A2) to (I-Al).

111. The composition for use, use or method of claim 102, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A2) to (I- A3).

112. The composition for use, use or method of claim 111, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A2) to (I- A3).

113. The composition for use, use or method of claim 112, wherein the mixture has a molar ratio of 1.22: 1 of (I-A2) to (I- A3).

114. The composition for use, use or method of claim 112, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-Al) to (I-A3).

115. The composition for use, use or method of claim 114, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-Al) to (I-A3).

116. The composition for use, use or method of claim 115, wherein the mixture has a molar ratio of from 0.72: 1 of (I-Al) to (I-A3).

117. The composition for use, use or method of claim 106, wherein the mixture has a molar percentage of (I-Al) of from 18.6% to 27.9% of (I-A2) of from 32.6% to 45.8%, and of (I-A3) of from 26.8% to 37.4%.

118. The composition for use, use or method of claim 117, wherein the mixture has a molar percentage of (I-Al) of 23.3%, a molar percentage of (I-A2) of 39.2%, and a molar percentage of (I- A3) of 32.1%.

119. The composition for use, use or method of claim 117, wherein the mixture has a molar ratio of (I-A1):(I-A2):(I-A3) of 1 : 1.7: 1.4.

120. The composition for use, use or method of claim 107, wherein the mixture of at least two compounds is a 50:50 mixture.

121. The composition for use, use or method of claim 108, wherein the mixture of (I-Al), (I- A2) and (I- A3) is selected from:LPC(O-16:0) 26.8% + LPC(O-18:0) 46.1% + LPC(O-18:1) 27.1%;LPC(O-16:0) 46% + LPC(O-18:0) 21% + LPC(O-18:1) 33%;LPC(O-16:0) 42% + LPC(O-18:0) 51% + LPC(O-18:1) 7%;LPC(O-16:0) 62% + LPC(O-18:0) 23.9% + LPC(O-18:1) 14.1%;LPC(O-16:0) 19.8% + LPC(O-18:0) 66% + LPC(O-18:1) 14.2%;LPC(O-16:0) 32.5% + LPC(O-18:0) 39.6% + LPC(O-18:1) 27.9%; or LPC(O-16:0) 34.1% + LPC(O-18:0) 41.5% + LPC(O-18:1) 24.4%.

122. The composition for use, use or method of claim 108, wherein the mixture of (I-Al), (I- A2) and (I-A3) comprises 90% w / v (I-Al).

123. The composition for use, use or method of claim 108, wherein the mixture of (I-Al), (I- A2) and (I-A3) comprises 90% w / v (I-A2).

124. The composition for use, use or method of claim 108, wherein the mixture of (I-Al), (I- A2) and (I-A3) comprises 90% w / v (I-A3).

125. The composition for use, use or method of claim 108, wherein the mixture of (I-Al), (I- A2) and (I-A3) additionally comprises one or more of (I-A4), (I-A5) and (I-A6).

126. The composition for use, use or method of any one of claims 1 to 87, wherein the compound of Formula (I- A) is of the structure (I-A4), (I-A5), or (I-A6).

127. The composition for use, use or method of any preceding claims, wherein the composition comprises a mixture of at least two compounds selected from the group consisting of (I-A4), (I-A5), and (I-A6).

128. The composition for use, use or method of any preceding claims, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6).

129. The composition for use, use or method of any preceding claims, wherein the at least one compound is selected from a compound of Formula (I-A4), (I-A5) or (I-A6).

130. The composition for use, use or method of any preceding claims, wherein the composition comprises a mixture of (I-A4), (I-A5), and (I-A6), wherein said mixture of (I-A4), (I-A5), and (I-A6) makes up at least 50% of the ether lipids in the composition on a molar percentage basis.

131. The composition for use, use or method of any preceding claims, wherein the mixture has a molar ratio of from 1.2: 1 to 2.5: 1 of (I-A5) to (I-A4).

132. The composition for use, use or method of claim 124, wherein the mixture has a molar ratio of from 1.5: 1 to 2.1 : 1 of (I-A5) to (I-A4).

133. The composition for use, use or method of claim 125, wherein the mixture has a molar ratio of 1.7: 1 of (I-A5) to (I-A4).

134. The composition for use, use or method of any preceding claims, wherein the mixture has a molar ratio of from 0.9: 1 to 1.7: 1 of (I-A5) to (I-A6).

135. The composition for use, use or method of claim 127, wherein the mixture has a molar ratio of from 1 : 1 to 1.5: 1 of (I-A5) to (I-A6).

136. The composition for use, use or method of claim 128, wherein the mixture has a molar ratio of 1.29: 1 of (I-A5) to (I-A6).

137. The composition for use, use or method of any preceding claims, wherein the mixture has a molar ratio of from 0.5: 1 to 1 : 1 of (I-A4) to (I-A6).

138. The composition for use, use or method of claim 130, wherein the mixture has a molar ratio of from 0.6: 1 to 0.9: 1 of (I-A4) to (I-A6).

139. The composition for use, use or method of claim 131, wherein the mixture has a molar ratio of 0.76: 1 of (I-A4) to (I-A6).

140. The composition for use, use or method of any preceding claims, wherein the mixture has a molar percentage of (I-A4) of from 18.6% to 27.9%, of (I-A5) of from 32.6% to 45.8%, and of (I-A6) of from 26.8% to 37.4%.

141. The composition for use, use or method of claim 133, wherein the mixture has a molar percentage of (I-A4) of 24.8%, a molar percentage of (I-A5) of 42.4%, and a molar percentage of (I-A6) of 32.8%.

142. The composition for use, use or method of claim 133, wherein the mixture has a molar ratio of (I-A4):(I-A5):(I-A6) of 1 : 1.7: 1.3.

143. The composition for use, use or method of claim 123, wherein the mixture of the at least two compounds is a 50:50 mixture.

144. The composition for use, use or method of claim 124, wherein the mixture of (I-A4), (I- A5) and (I-A6) is selected from:LPE(O-16:0) 26.8% + LPE(O-18:0) 46.1% + LPE(O-18: 1) 27.1%;LPE(O-16:0) 46% + LPE(O-18:0) 21% + LPE(O-18:1) 33%;LPE(O-16:0) 42% + LPE(O-18:0) 51% + LPE(O-18:1) 7%;LPE(O-16:0) 62% + LPE(O-18:0) 23.9% + LPE(O-18:1) 14.1%;LPE(O-16:0) 19.8% + LPE(O-18:0) 66% + LPE(O-18:1) 14.2%;LPE(O-16:0) 32.5% + LPE(O-18:0) 39.6% + LPE(O-18:1) 27.9%; orLPE(O-16:0) 34.1% + LPE(O-18:0) 41.5% + LPE(O-18:1) 24.4%.

145. The composition for use, use or method of claim 128, wherein the mixture of (I-A4), (I- A5) and (I-A6) comprises 90% w / v (I-A4).

146. The composition for use, use or method of claim 128, wherein the mixture of (I-A4), (I- A5) and (I-A6) comprises 90% w / v (I-A5).

147. The composition for use, use or method of claim 128, wherein the mixture of (I-A4), (I- A5) and (I-A6) comprises 90% w / v (I-A6).

148. The composition for use, use or method of any one of claims 1 to 147, wherein the compound of Formula (I- A) is administered in a dose of from 0.1 to 4000 mg per day.

149. The composition for use, use or method of claim 148, wherein the compound of Formula (I- A) is administered in a dose of from 0.1 to 2000 mg per day.

150. The composition for use, use or method of claim 148, wherein the compound of Formula (I- A) is administered in a dose of from 25 to 1600 mg per day.

151. The composition for use, use or method of claim 148, wherein the compound of Formula (I- A) is administered in a dose of 400 mg, 800 mg, or 1600 mg per day.

152. The composition for use, use or method of claim 148, wherein the compound of Formula (I-A) is administered in a dose of 200 mg per day.

153. The composition for use, use or method of claim 148, wherein the compound of Formula (I-A) is administered in a dose of from 25 to 100 mg per day.

154. The composition for use, use or method of claim 148, wherein the compound of Formula (I-A) is administered in a dose of 25 mg, 50 mg, or 100 mg per day.

155. The composition for use, use or method of claim 148, wherein the compound of Formula (I-A) is administered in a dose of 30 mg, 100 mg, or 300 mg per day.

156. The composition for use, use or method of any one of claims 1 to 155, wherein the composition is a pharmaceutical composition.

157. The composition for use, use or method of any one of claims 1 to 155, wherein the composition is a pharmaceutical formulation.

158. The composition for use, use or method of any one of claims 1 to 155, wherein the composition is a food.

159. The composition for use, use or method of any one of claims 1 to 155, wherein the composition is dietary supplement.

160. The composition for use, use or method of any one of claims 1 to 155, wherein the composition is a medicinal food.

161. The composition for use, use or method of any one of claims 1 to 160, wherein the composition is suitable for oral administration.

162. The composition for use, use or method of claim 161, wherein the oral administration form is a tablet, a capsule, a solution, a mouthwash, a suspension, a powder, a gum, a confectionary, a lozenge, a sublingual delivery system, or a rapid-melt formulation.

163. The composition for use, use or method of any one of claims 1 to 162, wherein the composition comprises at least one of a solubilizing agent, an emulsifier, a stabilizer, a dispersal agent, an antioxidant, an antifoaming agent, or a diluent.

164. The composition for use, use or method of claim 163, wherein the composition comprises at least one solubilizing agent.

165. The composition for use, use or method of claim 164, wherein the solubilizing agent is selected from the group consisting of carboxymethylcellulose sodium, hypromellose, proline, xanthan gum, maltodextrin, alginates, waxes, lipids, oils, alcohols, sugars, microcrystalline cellulose, starches, calcium phosphates, mannitol, sorbitol, erythritol, food grade solvents, phospholipids, DMSO, ethanol, ethyl acetate, and isopropanol.

166. The composition for use, use or method of any one of claims 85 to 165, wherein the liver disease is selected from non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver steatosis, hepatitis, liver fibrosis, cirrhosis, and liver cancer.

167. The composition for use, use or method of any one of claims 85 to 166, wherein the treating, preventing, or protecting against liver disease comprises treating, preventing, or protecting against one or more symptoms of the liver disease.

168. The composition for use, use or method of any one of claims 85 to 167, wherein the liver disease is non-alcoholic fatty liver disease (NAFLD).

169. The composition for use, use or method of any one of claims 85 to 167, wherein the liver disease is non-alcoholic steatohepatitis (NASH).

170. The composition for use, use or method of claim 168, wherein the NAFLD is progressive with increased steatosis, increased inflammation, increased fibrosis, or increased cirrhosis.

171. The composition for use, use or method of claim 168, wherein the NAFLD is stable with preserved liver function.

172. The composition for use, use or method of any of claims 168-171, wherein the NAFLD is metabolic dysfunction-associated steatotic liver disease (MASLD).

173. The composition for use, use or method of claim 172, wherein the composition comprises a lysoalkylphosphatidylethanolamine.

174. The composition for use, use or method according to claim 167, wherein the treating, preventing, or protecting against the one or more symptoms of liver disease comprises improvements in liver function.

175. The composition for use, use or method of any one of claims 85 to 174, wherein the treating, preventing, or protecting against liver disease comprises treating, preventing, or protecting against liver steatosis, hepatitis, liver fibrosis, or liver cirrhosis.

176. The composition for use, use or method of any one of claims 85 to 174, wherein the treating, preventing, or protecting against the liver disease results in improvements in the liver function based upon changes in liver mass, liver lipids (e.g., triglyceride), expression of markers of liver fibrosis (e.g., Collal), liver inflammation (e.g.,TNF alpha), and fatty acid oxidation gene expression (e.g., CPTla, Acoxl) liver imaging, blood metabolic panels, or blood liver protein levels.

177. The composition for use, use or method of any one of claims 85 to 174, wherein the treatment lowers the HOMA-insulin resistance score and / or restores hepatic insulin signalling, and / or regulation of glucose homeostasis in a subject.

178. The composition for use, use or method of any one of claims 85 to 174, wherein the treatment provides upregulated expression of lrs2 and downregulated expression of G6pc indicative of lowered insulin resistance and / or treatment of insulin resistance.

179. The composition for use, use or method of claim 176, wherein the liver function is determined by serum levels of aspartate aminotransferase (AST), alanineaminotransferase (ALT), C reactive protein (CRP), triglyceride (TG), and HDL-C, LDL-C and total cholesterol.

180. The composition for use, use or method of claim 176, wherein the liver inflammation is determined by serum and hepatic expression of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin- 1 (IL-1) levels.

181. The composition for use, use or method of any one of claims 85 to 180, wherein treating the liver disease comprises improvements in liver steatosis, liver inflammation (i.e., hepatitis), liver fibrosis, cirrhosis, or liver metabolism.

182. The composition for use, use or method of any one of claims 85 to 181, wherein treating the liver disease comprises an improvement in of serum levels of plasmalogens (e.g., lyso species), phospholipids (e.g., phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol), sphingolipids (e.g., ceramides, glycosphingolipids and sphingomyelins), glycerolipids (e.g., diacyl- and triacylglycerols), cholesterol, cholesterol esters, and free fatty acids.

183. The composition for use, use or method of claim 176, wherein the liver disease is measured by imaging to determine the extent of liver remodelling associated with steatosis, fibrosis, and cirrhosis.

184. The composition for use, use or method of any one of claims 1-183, wherein the treatment further comprises the use or administration of one or more alkylglycerols.

185. The composition for use, use or method of claim 184, wherein the composition further comprises the one or more alkylglycerols.

186. The composition for use, use or method of any one of claims 1-185, wherein the treatment further comprises the use or administration of one or more omega-3 fatty acids, such as DHA, ALA, and / or EP A; and one or more omega-6 fatty acids, such as ARA.

187. The composition for use, use or method of any one of claims 1-186, wherein the treatment further comprises the use or administration of one or more PC(O)s and / or PE(O)s, for example wherein the composition comprises the one or more PC(O)s and / or PE(O)s.

Images