Dietary supplement particularly indicated for the prevention of cognitive decline, capsule comprising said supplement, and its use

Abstract

The present invention relates to a dietary supplement indicated for the treatment of macular degeneration, more specifically a dietary supplement designed to assist in combating macular degeneration. The formulation is based on fish oil (a source of omega-3 TG) combined with cysteine, taurine, lutein, zeaxanthin, and vitamins, supporting visual health through a synergistic action of its components, enhanced by the benefits of omega-3. The present invention also relates to a capsule comprising said dietary supplement and the use of said supplement for combating macular degeneration.

Description

“FOOD SUPPLEMENT PARTICULARLY INDICATED FOR THE PREVENTION OF COGNITIVE DECLINE, CAPSULE COMPRISING SAID SUPPLEMENT AND ITS USE” FIELD OF APPLICATION

[0001] . The present invention belongs to the Food technology sector and refers to a food supplement for preventing cognitive decline, more specifically to a food supplement comprising compounds to help prevent cognitive decline, developed based on fish oil (source of Omega 3-TG), with a combination of: vitamins, minerals and phosphatidylserine, which act synergistically in its composition added to the benefits of omega-3.

[0002] . Furthermore, the present invention relates to a capsule comprising said dietary supplement and the use of said supplement for preventing cognitive decline. BACKGROUND OF THE INVENTION

[0003] It is estimated that more than 24 million people worldwide have dementia syndromes, with the global prevalence ranging from 5 to 10%. In Brazil, the prevalence is estimated at 5 to 19% according to a recent systematic review, with an increase as age increases (ranging from 0.5% to 2% at age 60 to 25% over age 85). The prevalence of dementia has also been growing worldwide, predominantly in developing countries like Brazil, becoming a major public health challenge. This growth is largely driven by the aging population that has been a hallmark of modern society. Recent studies estimate that there are more than 810 million older individuals (60 years or older), constituting 11.5% of the global population. By 2050, an estimated two billion older adults will be living, or 22% of the global population. INCORPORATED BY REFERENCE (RULE 20.6)

[0004] With aging, several physiological changes occur in the central nervous system, such as a reduction in brain mass, dendritic synapses, and even the volume of the prefrontal cortex. However, these changes are considered normal and do not significantly affect the elderly's memory.

[0005] . Currently, even with evidence of a decrease in the incidence of premature aging, the number of dementia cases is expected to approximately double every 20 years, rising to 115 million by 2051. As a result, lifestyle strategies to preserve or improve memory and cognition have provided significant health, social, and economic benefits. Data show, for example, that in the United Kingdom, delaying the onset of dementia by 2 or 5 years would result in 19% and 33% reductions in prevalence, respectively, by 2050, with a much lower prevalence of severe dementia. Similarly, it has been estimated that a 2-year delay in onset would reduce the global incidence of dementia by 22% by 2047, resulting in 25 million fewer cases.

[0006] The neural processes involved in cognitive decline are complex and multifactorial, and to date, nutritional intervention approaches are reductionist, often focusing on the impact of individual foods, food groups, or dietary components on cognitive function. Therefore, combined treatments with dietary compounds that target multiple physiological and molecular mechanisms may likely contribute to cognition.

[0007] Among dementias, the most common is Alzheimer's disease, which accounts for 50% of cases and whose treatment is based on symptom control. However, early diagnosis can bring benefits to the individual, their family, and the healthcare system.

[0008] . Elderly people have more chronic-degenerative diseases, which requires continuous monitoring and interventions, more assistance INCORPORATED BY REFERENCE (RULE 20.6) frequent in health services, impacting primary care. In addition to a greater number of hospital interventions, patients spend longer in bed than other age groups.

[0009] Among the most common diseases in the elderly is dementia, a public health problem because it causes economic and social impacts and impacts on the quality of life of the individual and society.

[0010] Phosphatidylserine is an endogenous, naturally occurring phospholipid, an essential component with a structural role in maintaining the integrity of cell membranes and important regulatory functions in mammalian cells. Its highest concentration is found in the brain, where it accounts for approximately 15% of the total phospholipid pool. It also plays a fundamental role in the function and homeostasis of neuronal cell membranes, significantly impacting the signaling process.

[0011] . Recent discoveries demonstrating the critical role of phosphatidylserine in activating important signal transduction pathways and modulating the release of specific neurotransmitters, including acetylcholine, norepinephrine, and dopamine, and receptor function, as well as implications in neuropathology, have further increased the interest of phosphatidylserine in relation to brain function.

[0012] . We highlight below some teachings from the state of the art that refer to this matter:

[0013] . Document BR 11 2022 005980 9 refers to a method for improving cognition and / or treating cognitive decline in a cognitively healthy subject comprising administering to the cognitively healthy subject a therapeutically effective amount of a compound of formula I, such as Xanamem (also known as UE2343) or a pharmaceutically acceptable salt, solvate or prodrug thereof, as described herein.

[0014] . Now, document BR 11 2020 011345 0 reveals compositions that INCORPORATED BY REFERENCE (RULE 20.6) include cyclobenzaprine and methods for treating or preventing agitation, psychosis and / or cognitive decline and their associated symptoms in dementia and other neurodegenerative conditions.

[0015] . Document BR 11 2020 000963 6 discloses compositions and methods for treating and preventing cognitive decline in individuals. These compositions comprise gotu kola or an extract thereof; tocopherol or a derivative thereof; ginseng or an extract thereof; a selenium compound; and α-lipoic acid. Methods for producing such compositions are also disclosed.

[0016] . Document BR 11 2019 018729 4 discloses a method of mitigating, treating, or preventing cognitive aging in an individual who does not have dementia that includes administering to the individual a therapeutically effective amount of a composition containing an omega-3 fatty acid, a nitric oxide-releasing compound, vitamin B12, and choline. The composition is administered at a daily dose that provides 0.1 to 50 times the recommended daily intake (RDA) of vitamin B12 per day, more frequently 0.1 to 40 times the recommended daily intake (RDA) of vitamin B12 per day and 0.01 to 10 times the recommended daily intake (RDA) of choline. Optionally, vitamin B6 and / or vitamin B9 may be included in the composition. The method may provide a benefit that is one or more of decreased brain atrophy, increased or maintained number of synapses, increased phagocytosis of B-amyloid, or decreased or maintained neuroinflammation in the individual without dementia.The method can prevent dementia in an individual at risk of it, for example, an elderly human being.

[0017] . Therefore, as can be seen below, there is no solution in the state of the art equivalent to that presented here in the present invention that combines technical differences, economic advantages, safety and reliability. INCORPORATED BY REFERENCE (RULE 20.6) OBJECTIVES OF THE INVENTION

[0018] . The objective of the present invention is to provide a dietary supplement that enables normal brain development; protecting it against exposure to alcohol and infections, as well as mitigating intellectual disability by improving neural / cognitive functioning.

[0019] . The object of the present invention is to provide a food supplement particularly indicated for the prevention of cognitive decline due to macular degeneration that can be administered in a 1.5g capsule. SUMMARY OF THE INVENTION

[0020] . The present invention achieves these and other objectives through a dietary supplement for preventing cognitive decline that comprises fish oil, silicon dioxide, soy lecithin, phosphatidylserine, vitamin B6, selenium yeast, magnesium bisglycinate, vitamin B3, vitamin B12, vitamin E.

[0021] . Furthermore, the present invention achieves these and other objectives by means of a capsule comprising the above supplement.

[0022] . Furthermore, the present invention achieves these and other objectives through the use of said supplement to prepare the capsule for preventing cognitive decline. DETAILED DESCRIPTION OF THE INVENTION

[0023] . The present invention is a food supplement for the prevention of cognitive decline comprising fish oil, silicon dioxide, soy lecithin, phosphatidylserine, vitamin B6, selenium yeast, magnesium bisglycinate, vitamin B3, vitamin B12, vitamin E.

[0024] . In a preferred embodiment of the present invention, said supplement comprises: - fish oil being fish oil 3020 TG liquid in an amount of 0.42 g; INCORPORATED BY REFERENCE (RULE 20.6) - silicon dioxide powder in an amount of 0.03g; - soy lecithin being phosphatidyl cholle 35% liquid in an amount of 0.17g; - phosphatidylserine being phosphatidylserine 70% in powder form in an amount of 0.07g; - vitamin B6 being pyridoxine hydrochloride powder in an amount of 0.007g; - selenium yeast powder in an amount of 0.0125g; - magnesium bisglycinate being magnesium bisglycinate 18% in powder form in a quantity of 0.12g; - vitamin B3 being niacinamide powder in an amount of 0.01g; - vitamin B12 being methylcobalamin in an amount of 0.00005g; - vitamin E being tocopherol acetate in an amount of 0.01g.

[0025] . Preferably, the acceptable vehicle is water.

[0026] . Further, the present invention may comprise gelatin being bovine edible gelatin (21) bloom) in an amount of 0.22g, glycerin being liquid USP double distilled vegetable glycerin in an amount of 0.09g, water in an amount of 0.19g and annatto oil (color) in an amount of 0.1g.

[0027] . The present invention, in a preferred embodiment, is administered by the user in a 1.5g capsule.

[0028] The dietary supplement for preventing cognitive decline of the present invention offers enormous advantages, in that a healthy dietary pattern can affect mental health and well-being through antioxidant, anti-inflammatory, neurogenic, microbiome and immune system modifying mechanisms, as well as through epigenetic modifications. Furthermore, the dietary profile affects not only INCORPORATED BY REFERENCE (RULE 20.6) only the composition, structure and function of the brain, but also endogenous hormones, neuropeptides, neurotransmitters and the gut-brain axis of the microbiota, playing a fundamental role in the modulation of stress, inflammation and in the prevention of cognitive function.

[0029] . In addition to a balanced diet, micronutrient supplementation, macronutrients, such as fatty acids, can provide beneficial effects due to their diverse biological functions.

[0030] Phosphatidylserine: Exogenous phosphatidylserine supplementation has shown benefits in mental performance, where it is known to improve brain functions, including long-term memory and recognition, especially in the elderly. Phosphatidylserine supplementation has shown improvement in elderly individuals with cognitive decline due to Alzheimer's disease, and phosphatidylserine also has an effect on younger individuals. They showed that individuals who received phosphatidylserine supplementation felt less stressed and had a better mood during cognitive tasks.

[0031] Clinical trials suggest that phosphatidylserine may have applications in the prevention and treatment of age-related cognitive decline, Alzheimer's disease, depression, and other cognitive disorders. More than 35 clinical trials of phosphatidylserine have been conducted in the United States and Europe: 11 of them were double-blind, randomized, placebo-controlled studies. Most studies focused on the effect of phosphatidylserine on memory and cognition in elderly patients with varying degrees of cognitive impairment.

[0032] . Exogenous phosphatidylserine supplementation has shown benefits in mental performance, where it is known to improve brain functions, including long-term memory and recognition, especially in the elderly.

[0033] . Based on this, a body of evidence supports the meaning INCORPORATED BY REFERENCE (RULE 20.6) Functional role of phosphatidylserine in the brain. The underlying mechanisms are still evolving; however, phosphatidylserine facilitates the activation of signaling proteins and receptors that are critical for neuronal survival, differentiation, and synaptic neurotransmission. Despite its constitutive nature, membrane phosphatidylserine is often an indispensable participant in signaling events and / or influences signaling in a concentration-dependent manner. The recommended dosage of phosphatidylserine for the treatment of cognitive impairment in adults is 300 mg / day orally, usually in divided doses. As a preventive measure, 100 mg / day is generally recommended.

[0034] Omega-3: The omega-3 essential fatty acid derived from docosahexaenoic acid (DHA) is one of the two main fatty acids found in the 2-position of phosphatidylserine derived from the bovine cerebral cortex. Since soybean products do not contain docosahexaenoic acid, it would be advisable to increase the consumption of cold-water fish (e.g., salmon, mackerel, and herring) or consider taking fish oil capsules to ensure adequate intake of this fatty acid while supplementing with phosphatidylserine. The brain is enriched with DHA, and the phosphatidylserine content in the gray matter of the human brain is particularly high; that is, phosphatidylserine levels are highest in the brain, where DHA is abundant. 4 In contrast, depletion of DHA in the brain reduces phosphatidylserine levels.

[0035] For example, dietary depletion of n-3 fatty acids can reduce brain DHA and increase n-6 fatty acids. Because n-6 fatty acid-containing phospholipids are not as good substrates for phosphatidylserine synthesis as DHA-containing phospholipid species, brain phosphatidylserine levels are reduced. It is important to note that modern Western diets are overly abundant in n-6 fatty acids compared to n-3 fatty acids, and therefore, DHA enrichment in the brain is compromised. INCORPORATED BY REFERENCE (RULE 20.6)

[0036] . Consistent with the preference for DHA-containing substrates in phosphatidylserine biosynthesis, evidence from neuronal cell cultures also suggests that phosphatidylserine and DHA prevent apoptosis through a common mechanism. Consistently, hippocampal neurons from DHA-depleted animals showed reduced amounts of phosphatidylserine and were more susceptible to cell death.

[0037] . A decrease in DHA and phosphatidylserine content has been reported in cognitive impairment4. A small reduction in the DHA content of hippocampal phosphatidylserine was observed in 12-month-old accelerated senescence-prone mice that have a shorter lifespan, learning and memory deficits.

[0038] Similarly, cognitive improvement was reported in humans given oral phosphatidylserine supplements, and these findings were later confirmed and expanded. Humans treated for 42 days with 200 mg of soy-based phosphatidylserine showed a more relaxed state before and after mental stress measured by electroencephalography, and no adverse effects were evident at this dose administered three times daily for 6 to 12 weeks. Word recall increased by 42% in male and female individuals over 60 years of age who complained of subjective memory loss when treated with 300 mg / day of phosphatidylserine containing 37.5 mg of eicosapentaenoic acid and DHA. Improvement in immediate verbal recall was also observed in a double-blind, placebo-controlled clinical trial in a large group of elderly individuals with memory complaints when treated with a daily dose of 300 mg of phosphatidylserine containing DHA and eicosapentaenoic acid.A subset with relatively good cognitive performance at baseline showed the greatest improvement.

[0039] . Therefore, the biosynthesis of phosphatidylserine utilizes INCORPORATED BY REFERENCE (RULE 20.6) preferably phospholipids containing DHA as substrate and the level of phosphatidylserine can be altered according to the concentration of DHA, specifically in the brain.

[0040] Recent evidence from short-term trials suggests that EPA treatment may be relevant for cognitive function in healthy adults. Possibly supporting these effects, emerging evidence suggests that EPA may improve neural efficiency and increase prefrontal cortex hemoglobin oxygenation during cognitive tasks. Furthermore, a pilot study evaluating the effects of 20 weeks of daily DHA + EPA supplementation found that the observed improvement in neurovascular coupling on a battery of cognitive tests after the intervention correlated with increases in red blood cell EPA concentrations.

[0041] Another randomized, placebo-controlled, double-blind study revealed that after 26 weeks of supplementation with EPA-rich oil, global cognitive function improved in terms of speed and accuracy, as well as significantly increased accuracy in performing all memory tasks. These results extend previous findings in healthy older adults, where observational data revealed a positive relationship between EPA status and global cognitive function, and beneficial effects of EPA-rich treatments on executive functions were also observed. Collectively, these findings are interesting because they suggest that although EPA is stored in the brain in low amounts, it may still play an important role in cognitive functions.

[0042] In conclusion, EPA-rich oil improved global cognitive function in healthy young adults who routinely consumed small amounts of oily fish. The findings also provide further evidence that EPA supplementation and INCORPORATED BY REFERENCE (RULE 20.6) DHA may positively influence neural efficiency.

[0043] . Thus, an adequate intake of omega-3 may delay age-related mild cognitive impairment and protect against the risk of neurodegenerative dementia, and higher plasma EPA + DHA levels are associated with less decline in cognition and memory.

[0044] EPA and DHA have anti-inflammatory properties and exert diverse biological activities. DHA is highly concentrated in the central nervous system, where it plays a fundamental role in cognitive development and function. However, with aging, this concentration declines, which is particularly concerning in Western countries, as omega-3 intake is considerably low between healthy aging and dementia, characterized by cognitive deficits along with intact daily activities. Excessive neuroinflammation associated with the aging process can affect brain regions known to support learning and memory, contributing to mild cognitive impairment.

[0045] Neuropsychiatric disorders have traditionally been linked to dysregulation of neurotransmitters such as dopamine, norepinephrine, glutamate, and serotonin, contributing to their mood and cognitive dysfunction. However, the persistence of treatment-resistant conditions has led to the hypothesis of a relationship between inflammation and neuropsychiatric disorders, supported by the association with chronic inflammatory and immunological processes.

[0046] . Furthermore, peripheral immune modulators, such as pro-inflammatory interleukin-113 (IL-1(3)) and tumor necrosis factor-α (TNF-α), can induce psychiatric symptoms in animal models. Finally, peripheral cellular and humoral immune abnormalities are more prevalent in psychiatric individuals versus controls. INCORPORATED BY REFERENCE (RULE 20.6) healthy. Neuroinflammation represents a central nervous system reaction to events that interfere with tissue homeostasis and is present in virtually all neurological diseases. Furthermore, oxidative stress caused by reactive oxygen / nitrogen species and mitochondrial disorders play fundamental roles in neuroinflammation. Due to its composition and biochemical characteristics, the brain is particularly vulnerable to oxidative stress, which can induce cerebral lipid peroxidation, damage to membrane phospholipids and neurotransmitter receptors, and depletion of endogenous antioxidants.

[0047] EPA and DHA have a well-known effect on the synthesis, release, receptor function, and storage of neurotransmitters during development and in neuropsychiatric disorders. Regarding inflammatory reactions, DHA and EPA generally exert an inhibitory effect on the activation of immune cells of both the innate and adaptive systems. In particular, omega-3s can act as signaling molecules and decrease cytokine secretion by macrophages, suppressing inflammation. DHA and EPA can also decrease neutrophil migration and increase their phagocytic capacity. It is noteworthy that during increased vascular wall permeability, plasma omega-3 PlIFAs reach the site of inflammation, potentially blocking chronic inflammation and reducing fibrosis.A national survey conducted in the United States indicated a significant association between EPA+DHA intake in the last 24 hours and a 25% reduced prevalence of depressive symptoms in a sample of 10,480 adults.

[0048] Choline: Choline is an essential nutrient for brain, liver, and muscle function. It is a major constituent of cell membranes and organelles and plays a vital role in physiological processes, including histone methylation and signal transduction. INCORPORATED BY REFERENCE (RULE 20.6) nerve myelination.

[0049] Metabolically, choline is involved in the synthesis of acetylcholine, phospholipids, and betaine. Choline is a necessary precursor for the synthesis of acetylcholine, a neurotransmitter involved in functions related to memory and muscle control. Therefore, due to its metabolic role, choline is important for cognitive function. In addition to the synthesis of the neurotransmitter acetylcholine, it is necessary for the synthesis of phosphatidylserine, which is essential for membrane integrity and the maintenance of brain structure and function.

[0050] Adequate choline intake is important to maintain brain integrity and functionality. There is a specific mechanism for active choline transport across the blood-brain barrier, and this cerebral choline transport capacity, which is proportional to serum concentrations, determines the synthesis of the neurotransmitter acetylcholine. Furthermore, choline administration appears to promote greater brain phosphatidylcholine synthesis, and lower choline intake increases the likelihood of decreased brain phospholipid and acetylcholine synthesis, which increases the risk of impaired cognitive function.

[0051] There are several follow-up studies that have analyzed the relationship between dietary choline and cognitive function—the association between choline intake, cognitive function, and brain morphology in a cohort of 1,391 adults without dementia. Choline intake was positively associated with verbal and visual memory, while early-life intake of the vitamin was associated with less brain atrophy.

[0052] However, both total choline and phosphatidylcholine intake were associated with improved cognitive performance on verbal fluency and memory tests.

[0053] . Therefore, choline has recently been named as a neuroprotectant and collectively the evidence shows choline as a INCORPORATED BY REFERENCE (RULE 20.6) A neurocognitive nutrient essential for normal brain growth and function. Furthermore, there is a body of evidence from animal studies, which is increasingly being reinforced by human trials, suggesting three broad pillars of potential benefit for choline supplementation: - support normal brain development; - protect against alcohol exposure and infections; - mitigate intellectual disability by improving neural / cognitive functioning and memory.

[0054] Vitamin E: Vitamin E is essential for neurological development and is one of the best-known and most effective nutrients for modulating immune function. A deficiency can impair this function and increase the risk of neurological abnormalities or disorders. In situations where neuroinflammation is significant, vitamin E supplementation can modulate this oxidative stress.

[0055] Vitamin E exerts protective antioxidant and anti-inflammatory activity, effectively preventing lipid peroxidation. It accumulates particularly in areas where free radical production is highest, such as mitochondrial membranes.

[0056] . Magnesium: Magnesium is the second most abundant intracellular mineral and is necessary as a cofactor for more than 300 enzymatic reactions, being essential for the biochemical functioning of several metabolic pathways in the body, including cellular energy metabolism, gene regulation, maintenance of bones and teeth, nerve conduction, membrane stability and synaptic transmission, therefore, important for the proper functioning of the brain and nervous system.

[0057] . In addition, magnesium has anti-inflammatory properties, as it plays a fundamental role in INCORPORATED BY REFERENCE (RULE 20.6) The differentiation, proliferation, functioning, and movement of immune cells is important for balanced responses of these cells. In fact, some studies have revealed a positive effect of magnesium in reducing neuroinflammation, increasing the progression of cognitive impairment and dementia.

[0058] . Furthermore, magnesium supplementation has been shown to improve migraines, depression, Alzheimer's disease, stroke, and also benefit anxiety in individuals prone to mental stress.

[0059] Vitamin B3: Vitamin B3 has also been studied for depression, as 60 mg of tryptophan forms 1 mg of niacin equivalent in the kynurenine pathway, and B3 supplementation could spare tryptophan. Niacin also acts as an electron carrier in oxidation-reduction reactions. In addition to its role in energy metabolism, B3 may help control dyslipidemia, especially through its action in increasing HDL and reducing triglycerides. Another application of this vitamin is in the process of mitochondrial biogenesis.

[0060] Vitamin B6: Vitamin B6 plays a role in approximately 100 enzymatic reactions, 40% of which are transamination reactions. This vitamin is involved in the synthesis of hormones and neurotransmitters such as serotonin, dopamine, and GABA. Because of this role, its deficiency is associated with depression, anxiety, irritability, premenstrual tension, and binge eating.

[0061] Vitamin B12: Some preclinical studies have reported a choline-sparing effect with vitamin B12 supplementation, and patients with B12 deficiency have also shown lower blood choline concentrations. Therefore, these data provide a relevant rationale for combining formulations containing choline with vitamin B12.

[0062] . Selenium: selenium has antioxidant and numerous other properties. INCORPORATED BY REFERENCE (RULE 20.6) Selenium has important functions, and therefore, its adequate consumption is associated with a lower risk of chronic diseases, such as cardiovascular disease, diabetes, and Alzheimer's disease, in addition to its well-established role in thyroid health. Selenium also plays an important role in the detoxification of heavy metals, especially mercury, cadmium, and arsenic.

[0063] Selenium also plays an important role in the proper functioning of the immune system, contributing to phagocytosis, natural killer cell activity, lymphocyte proliferation, and immunoglobulin synthesis. Based on this, selenium consumption can improve the antioxidant system and thus have positive effects on cognitive function. Furthermore, selenium supplementation was able to reduce oxidative stress and improve learning and memory function in specific behavioral tests. Therefore, in summary, the review showed a strong correlation between selenium consumption and improved cognitive performance.

[0064] . Therefore, the present invention synergistically combines compounds that act uniquely for the purpose presented here:

[0065] . Phosphatidylserine: - Phospholipid with highest concentration in the brain; - Homeostasis of neuronal cell membranes; - Benefits in cognitive performance.

[0066] . Hill: - Neuroprotective; - Essential neurocognitive nutrient for normal brain growth and function.

[0067] . Omega 3: - Helps with neuroinflammation; INCORPORATED BY REFERENCE (RULE 20.6) - Adequate intake can delay cognitive impairment; - Reduces stress, anxiety and depression.

[0068] . Vitamins and minerals: - Essential for neurological development; - Help with neuroinflammation; - Contribute to good neurological functioning and improve cognitive performance; - Reduces inflammation, oxidative stress and anxiety.

[0069] . Having described an example of a preferred embodiment of the present invention, it should be understood that the scope of the present invention encompasses other possible variations of the inventive concept described, being limited only by the content of the appended claims, including possible equivalents. INCORPORATED BY REFERENCE (RULE 20.6) “FOOD SUPPLEMENT PARTICULARLY INDICATED FOR COMBATING MACULAR DEGENERATION, CAPSULE COMPRISING SAID SUPPLEMENT AND ITS USE” FIELD OF APPLICATION

[0001] . The present invention belongs to the food technology sector and refers to a food supplement indicated for combating macular degeneration, more specifically a food supplement to help combat macular degeneration, developed based on fish oil (source of omega 3-TG) with a combination of cysteine, taurine, lutein, zeaxanthin and vitamins, helping with vision health, which act synergistically in its composition added to the benefits of omega-3.

[0002] . Furthermore, the present invention relates to a capsule comprising said food supplement and the use of said supplement to combat macular degeneration. BACKGROUND OF THE INVENTION

[0003] . Human aging is associated with a series of metabolic changes that predispose to the development of chronic degenerative diseases. Among the diseases that affect the elderly, those that compromise vision stand out. The most severe of these is Age-Related Macular Degeneration (AMD), which leads to severe vision loss and has no effective treatment available on the market. AMD, like other chronic morbidities, is associated with changes in cellular metabolism, particularly oxidative stress and inflammation. In addition, purinergic signaling, still little studied in this disease, is directly associated with the oxidative and inflammatory processes. Therefore, it is important to understand the relationship between the purinergic system and the main processes. MISTAKENLY PRESENTED (RULE 20.5 bis) associated with the development of AMD.

[0004] . Age-Related Macular Degeneration (AMD) is a degenerative change in the main region of the retina, the macula, responsible for refined, refined central visual acuity (VA) that allows for seeing details that typically affects individuals over 60 years of age and that includes changes in the retinal pigment epithelium (RPE) such as hypo or hyperpigmentation, associated with drusen, in the initial phases, and may progress to complete atrophy of the RPE and choriocapillaris (geographic atrophy) or also to the development of choroidal neovascularization and consequent subretinal fibrous scar, called disciform scar, in its initial phases.

[0005] . Due to the involvement of the macula, the patient presents distorted and blurred central vision with significant impairment of visual function, significantly impacting their daily activities and quality of life.

[0006] . The pathophysiology of AMD is multifactorial, complex, and still not completely understood. Age-related changes, a complex metabolic and functional interaction, genetic, and environmental factors can contribute to the development of chronic changes in ocular structures in the macular region (choriocapillaris, Bruch's membrane, retinal pigment epithelium (RPE), and photoreceptors), which progress to different degrees of AMD. Oxidative stress, decreased choroidal circulation, changes in lipid metabolism, Bruch's membrane degeneration, and chronic inflammation are involved in the pathophysiology of AMD. Taking into account the clinical and pathological characteristics, AMD is classified into dry (atrophic) and wet (exudative, neovascular) forms.

[0007] . The dry form is characterized by the presence of drusen, progressive degeneration of the photoreceptors and changes in the RPE in the macular region. Drusen consist of deposits of abnormal material MISTAKENLY PRESENTED (RULE 20.5 bis) derived from the RPE in Bruch's membrane, due to the likely inability to clear waste in this region. The dry form can progress to geographic atrophy or the neovascular form.

[0008] . The neovascular form occurs due to the growth of blood vessels in the subretinal space, which originate from the choriocapillaris and grow through defects in Bruch's membrane, called subretinal neovascular membrane or choroidal neovascularization (CNV). CNV may be confined to the sub-RPE space or subsequently expand into the subretinal space. Extravasation from these neovessels leads to the accumulation of serous or serosanguineous content between the RPE and neurosensory retina.

[0009] . The molecule called vascular endothelial growth factor (VEGF) has been recognized as a key mediator in neovascular angiogenesis. This molecule promotes blood vessel proliferation and is considered the main agent responsible for the progression of the disease.

[0010] . AMD is one of the main causes of legal blindness in developed countries among individuals over 50 years of age, accounting for 5.93% of blindness cases worldwide. International data estimate that 18% of the population aged 65 to 74 years and 30% of the population aged 75 years or older have some stage of AMD. Statistical data in Brazil are scarce. With increasing life expectancy and an aging population, the prevalence of this condition is estimated to increase.

[0011] . The prevalence, incidence, and progression of all forms of AMD with age being the main risk factor. Smoking is the second main non-genetic risk factor.

[0012] . AMD is more prevalent in Caucasians. Other associated risk factors include family history, cardiovascular disease, high blood pressure, increased lipid intake, a diet low in omega-3s, and MISTAKENLY PRESENTED (RULE 20.5 bis) lutein-containing vegetables, obesity, and lack of physical activity. Multiple genes have been implicated in predisposition to the disease. The literature is inconclusive regarding risk factors such as light-colored irises and excessive sunlight exposure.

[0013] . The neovascular form accounts for 10% of all cases of the disease. However, it is responsible for approximately 80% of all cases of legal blindness attributed to AMD. This form is characterized by the formation of CNV, leading to rapid loss of central vision. CNV extends anteriorly through the RPE, leading to the accumulation of fluid and blood, or lipids, in the subretinal space.

[0014] . These side effects of the disease, combined with the presence of scar or fibrous tissue, cause a marked loss of central vision.

[0015] . Patients with exudative AMD present with complaints of sudden worsening of visual acuity, associated with metamorphopsia and central or paracentral scotomas.

[0016] . Clinically, CNV presents as a rounded, grayish lesion, associated or not with hemorrhages, hard exudates, and detachment of the neurosensory retina and / or RPE. In the final phase of the disease, the fibroblasts that accompany the growth of CNV organize themselves into fibrovascular tissue in the subretinal space, called a disciform scar.

[0017] . Exams used in the diagnosis and monitoring of AMD are fundoscopy, autofluorescence, fluorescein angiography and optical coherence tomography (OCT).

[0018] . Several literary references address several existing studies regarding nutrition in visual acuity and, therefore, several nutrients and their action have gained prominence in this new scenario such as: antioxidants (vitamins B, C and E), carotenes (lutein, zeaxanthin and carotene), zinc and polyunsaturated omega-3 fatty acids - acid MISTAKENLY PRESENTED (RULE 20.5 bis) docosahexaenoic acid (DHA) and its precursor eicosapentaenoic acid (EPA).

[0019] . For many experts, the use of supplements has seen significant growth as a way to promote health and prevent and treat chronic degenerative diseases. In recent years, an eye care aid has been studied: omega supplementation.

[0020] . Risk factors for macular degeneration include: age, family history, smoking, cardiovascular disease, hypertension, some genetic abnormalities, and sun exposure.

[0021] . There are two types of macular degeneration: dry and wet. - Dry macular degeneration: causes the macular tissues to become thinner as the cells disappear, and is the most common (85% of cases). - Wet macular degeneration: develops when abnormal blood vessels develop in front of the choroid, and is also the main cause of central vision loss.

[0022] . We highlight below some teachings from the state of the art that refer to the present matter:

[0023] . Document BR 11 2022 012676-0 deals with chemical compounds C that are derived from norbixin and have tropism for the eye, and are intended for use in the treatment of ocular diseases in mammals, in particular in the context of alteration of the retinal pigment epithelium and more particularly in the context of age-related macular degeneration (AMD) and Stargardt disease.

[0024] . Document BR 0410651-2 describes new thiotungstate derivatives, methods of manufacturing thiotungstate derivatives, pharmaceutical compositions containing thiotungstate derivatives to treat diseases associated with aberrant vascularization, copper metabolism disorder and obesity, neurodegenerative disorders or NF-kB dysregulation. MISTAKENLY PRESENTED (RULE 20.5 bis)

[0025] . Therefore, as can be seen below, there is no solution in the state of the art equivalent to that presented here in the present invention that combines technical differences, economic advantages, safety and reliability. OBJECTIVES OF THE INVENTION

[0026] . The objective of the present invention is to provide a food supplement based on fish oil (source of omega 3-TG), with a combination of: cysteine, taurine, lutein, zeaxanthin and vitamins, helping with vision health, which act synergistically in its composition, adding to the benefits of omega-3.

[0027] . It is a further objective of the present invention to provide a dietary supplement composition whose supportive therapy with lutein and zeaxanthin can have a beneficial effect in delaying the progression of eye diseases such as age-related macular degeneration (AMD) and cataracts.

[0028] . It is a further objective of the present invention to provide a dietary supplement composition with lutein beneficial for preventing the progression of AMD by increasing the optical density of the macular pigment, partially reversing visual loss in its early stages.

[0029] . The object of the present invention is to provide a food supplement particularly suitable for combating macular degeneration that can be administered in a 1.5g capsule. SUMMARY OF THE INVENTION

[0030] . The present invention achieves these and other objectives by means of a dietary supplement particularly indicated for combating macular degeneration that comprises fish oil, silicon dioxide, cysteine, lutein, zeaxanthin, vitamin B12, vitamin A, vitamin E, taurine and an acceptable vehicle.

[0031] . Furthermore, the present invention achieves these and other objectives by means of a capsule comprising the above supplement. MISTAKENLY PRESENTED (RULE 20.5 bis)

[0032] . Furthermore, the present invention achieves these and other objectives through the use of said supplement to prepare the capsule to combat macular degeneration. DETAILED DESCRIPTION OF THE INVENTION

[0033] . The present invention is a dietary supplement based on fish oil (source of omega 3-TG), with a combination of cysteine, taurine, lutein, zeaxanthin and vitamins A, E and B12, helping with vision health that act synergistically in its composition added to the benefits of omega-3. The present invention, therefore, relates to a dietary supplement particularly indicated for combating macular degeneration that comprises fish oil, silicon dioxide, cysteine, lutein, zeaxanthin, vitamin B12, vitamin A, vitamin E, taurine and an acceptable vehicle.

[0034] . In a preferred embodiment of the present invention, the dietary supplement particularly indicated for combating macular degeneration comprises: - fish oil comprising omega-3, with 1812 net TG present in an amount of 0.744g, - silicon dioxide powder in an amount of 0.06g, - cysteine ​​being N-acetyl cysteine ​​present in an amount of 0.03g, - lutein in an amount of 0.10g, - zeaxanthin being 10% zeaxanthin present in an amount of 0.01 g, - vitamin B12 being methylcobalamin 5% present in an amount of 0.000024g, - vitamin A being retinol acetate 500000 present in an amount of 0.00045g, - vitamin E being tocopherol acetate in an amount of 0.0075g, MISTAKENLY PRESENTED (RULE 20.5 bis) - taurine powder in an amount of 0.048g,

[0035] . Preferably, the acceptable vehicle is water.

[0036] . Further, the present invention may comprise glycerin being double distilled vegetable glycerin USP in an amount of 0.09g and gelatin being bovine edible gelatin (210) in an amount of 0.022g.

[0037] . The present invention may be comprised in a 1.5g capsule.

[0038] . As can be seen later, the present invention brings technical advantages over the state of the art because:

[0039] . Omega-3: Omega-3 fatty acids are a type of fat we need for health that our bodies cannot produce. The two main omega-3s with health benefits are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). They are found in animal sources, such as fatty fish.

[0040] . Lutein: Lutein is a substance linked to eye health, as it can offer protection against damage caused by visible light, helping to filter high-energy wavelengths found in blue light and protecting the eyes against the formation of reactive oxygen species and free radicals. Lutein, or lipochrome, is a lemon-yellow carotenoid found in some vegetables such as spinach, zucchini, cauliflower, peas, broccoli, and some fruits such as oranges, papayas, peaches, and kiwis, as well as egg yolks.

[0041] . Zeaxanthin: Zeaxanthin is a substance responsible for the color of fish, poultry, flowers, and food. It is found predominantly in yellow, orange, red, and green vegetables such as nectarines, oranges, papayas, peaches, broccoli, Brussels sprouts, cabbage, cauliflower, peas, corn, arugula, eggs, among others. This substance has numerous health benefits, such as preventing premature aging and protecting vision, as it is able to protect the eyes against MISTAKENLY PRESENTED (RULE 20.5 bis) UV rays emitted by the sun.

[0042] . Cysteine: Cysteine ​​is a non-essential amino acid produced by the body and is important for the formation of collagen and keratin. Cysteine ​​also has antioxidant properties and is important for the production of muscles, hormones, and enzymes, strengthening the immune system.

[0043] . For AMD, carotenoids and omega-3 fatty acids have also proven sufficient in preventing neurodegeneration.

[0044] . N-acetyl L-cysteine: is a derivative of the natural amino acid cysteine, which serves as a substrate for the synthesis of glutathione (GSH) in the body, which has an antioxidant effect. This reduces the formation of pro-inflammatory cytokines, such as IL-9 and TNF-a. GSH levels decrease with age and with certain health conditions, such as chronic non-communicable diseases.

[0045] . Taurine: Taurine, or 2-aminoethanesulfonic acid, is a sulfur-containing organic acid found in bile. It is one of the most abundant non-essential amino acids in our body, especially in the central nervous system, skeletal muscles, heart, brain, intestines, and skeletal bones. It has antioxidant and anti-inflammatory properties, helping to improve immunity, maintain eye health, and prevent premature aging.

[0046] . Vitamin E: Vitamin E is a fat-soluble vitamin essential for the body's functioning due to its antioxidant action and anti-inflammatory properties, which help improve the immune system, skin and hair, as well as prevent degenerative diseases.

[0047] . Vitamin A: Vitamin A helps fight free radicals, agents that accelerate cellular aging. This means it has antioxidant action, ensuring the preservation of various tissues, especially skin, mucous membrane, eye, and bone cells. MISTAKENLY PRESENTED (RULE 20.5 bis)

[0048] . Vitamin B12: Vitamin B12, also known as cyanocobalamin, is a very important vitamin for our body, as it is involved in the formation of our blood cells and acts directly on the nervous system, helping in the formation of neurons.

[0049] . In view of all the data, based on the results of studies evaluating the beneficial effects of compounds to aid in the treatment

[0050] . Supportive therapy with lutein and zeaxanthin may have a beneficial effect in slowing the progression of eye diseases such as age-related macular degeneration (AMD) and cataracts.

[0051] . High intake of specific nutrients, use of antioxidant supplements, and adherence to a Mediterranean diet decrease the risk of progression from early to late AMD.

[0052] . Lutein supplementation is beneficial in preventing the progression of AMD by increasing macular pigment optical density, partially reversing early-stage vision loss. It has proven to be an effective strategy in treating this disease, as a decrease in macular pigment optical density (MPOD) has been shown to be a determining factor in the onset of AMD in its more advanced stages.

[0053] . Lutein and zeaxanthin supplementation confers clinical benefit. However, it may be an appropriate preventive measure for patients at high risk of developing AMD. When compared with beta-carotene, lutein / zeaxanthin has a potentially beneficial association with late AMD progression.

[0054] . Having described an example of a preferred embodiment of the present invention, it should be understood that the scope of the present invention encompasses other possible variations of the described inventive concept, being limited only by the content of the appended claims, including possible equivalents. MISTAKENLY PRESENTED (RULE 20.5 bis)

Claims

CLAIMS 1. Food supplement for the prevention of cognitive decline characterized by comprising fish oil, silicon dioxide, soy lecithin, phosphatidylserine, vitamin B6, selenium yeast, magnesium bisglycinate, vitamin B3, vitamin B12, vitamin E.

2. Supplement according to claim 1, characterized in that the fish oil is liquid fish oil 3020 TG in an amount of 0.42 g.

3. Supplement according to claim 1 or 2, characterized in that silicon dioxide is in powder form in an amount of 0.03g.

4. Supplement according to any one of claims 1 to 3, characterized in that soy lecithin is phosphatidyl cholesteryl 35% liquid in an amount of 0.17g.

5. Supplement according to any one of claims 1 to 4, characterized in that phosphatidylserine is 70% phosphatidylserine powder in an amount of 0.07g.

6. Supplement according to any one of claims 1 to 5, characterized in that vitamin B6 is pyridoxine hydrochloride powder in an amount of 0.007g.

7. Supplement according to any one of claims 1 to 6, characterized in that selenium yeast is in powder form in an amount of 0.0125g.

8. Supplement according to any one of claims 1 to 7, characterized in that magnesium bisglycinate is 18% magnesium bisglycinate powder in an amount of 0.12g.

9. Supplement according to any one of claims 1 to 8, characterized in that vitamin B3 is niacinamide powder in an amount of 0.01 g.

10. Supplement according to any one of claims 1 to 9, characterized in that vitamin B12 is methylcobalamin in a INCORPORATED BY REFERENCE (RULE 20.6) quantity of 0.00005g.

11. Supplement according to any one of claims 1 to 10, characterized in that vitamin E is tocopherol acetate in an amount of 0.01 g.

12. Supplement according to any one of claims 1 to 11, characterized in that it comprises gelatin being bovine edible gelatin (21) bloom) in an amount of 0.22g.

13. Supplement according to any one of claims 1 to 12, characterized in that it comprises glycerin being liquid USP double-distilled vegetable glycerin in an amount of 0.09g.

14. Supplement according to any one of claims 1 to 11, characterized in that it comprises a dye being annatto oil in an amount of 0.1 g.

15. Capsule characterized by comprising a food supplement particularly indicated for preventing cognitive decline as defined in any one of claims 1 to 14.

16. Use of the dietary supplement as defined in any one of claims 1 to 14, characterized in that it is for preparing a capsule indicated for preventing cognitive decline. INCORPORATED BY REFERENCE (RULE 20.6) CLAIMS 1. Food supplement particularly indicated for combating macular degeneration characterized by comprising fish oil, silicon dioxide, cysteine, lutein, zeaxanthin, vitamin B12, vitamin A, vitamin E, taurine and an acceptable vehicle.

2. Supplement according to claim 1, characterized in that the fish oil comprises omega-3, being 1812 net TG and being present in an amount of 0.744g.

3. Supplement according to claim 1 or 2, characterized in that silicon dioxide is present in powder form in an amount of 0.06g.

4. Supplement according to any one of claims 1 to 3, characterized in that cysteine is N-acetyl cysteine present in an amount of 0.03g.

5. Supplement according to any one of claims 1 to 4, characterized in that lutein is present in powder form in an amount of 0.10g.

6. Supplement according to any one of claims 1 to 5, characterized in that 10% zeaxanthin is present in an amount of 0.01 g.

7. Supplement according to any one of claims 1 to 6, characterized in that vitamin B12 is 5% methylcobalamin and is present in an amount of 0.000024g.

8. Supplement according to any one of claims 1 to 7, characterized in that vitamin A is retinol acetate 500000 and is present in an amount of 0.00045g.

9. Supplement according to any one of claims 1 to 8, characterized in that vitamin E is present in an amount of 0.0075g.

10. Supplement according to any one of claims 1 to 9, characterized in that taurine is present in powder form in an amount MISTAKENLY PRESENTED (RULE 20.5 bis) of 0.048g.

11. Supplement according to any one of claims 1 to 10, characterized in that it comprises glycerin being double-distilled vegetable glycerin USP in an amount of 0.09g.

12. Supplement according to any one of claims 1 to 11, characterized in that it comprises gelatin being bovine edible gelatin (210) in an amount of 0.022g.

13. Capsule characterized by comprising a food supplement as defined in any one of claims 1 to 12.

14. Use of the food supplement as defined in any one of claims 1 to 12, characterized in that it is for preparing a capsule to combat macular degeneration. MISTAKENLY PRESENTED (RULE 20.5 bis)