177 results about "Neurodegeneration" patented technology

A method for identifying biomarkers indicative of neurodegeneration using a covariance neural network (VNN) includes providing a VNN trained on brain anatomical data primarily composed of healthy subjects, making the largest proportion of the population in the data. Brain anatomical data of a subject is provided as input, and, based on the input, the VNN generates a set of biomarkers and a brain health marker indicative of neurodegeneration of the subject.

The invention discloses a multi-modal medical image processing method and device, a storage medium and computer equipment. Comprising the following steps: performing three-dimensional discrete wavelet transform on a brain MRI image of a target patient to generate an MRI wavelet coefficient; inputting the MRI wavelet coefficient into a diffusion model to obtain a reference PET wavelet coefficient of the brain of the target patient in a healthy state; performing inverse wavelet transform on the reference PET wavelet coefficient to generate a reference PET image; and comparing the brain PET image of the target patient with the reference PET image, and determining the metabolic deviation index of the brain of the target patient. Therefore, each patient can take the condition without the neurodegenerative change as a contrast, space standardization does not need to be carried out on a group template, anatomical structure distortion caused by the space standardization is greatly reduced, voxel-level accurate analysis of the neurodegenerative disease is realized, tiny pathological change aiming at the patient can be identified, and the accuracy of voxel-level accurate analysis of the neurodegenerative disease is improved. And clinical doctors are assisted in early diagnosis.

The present application relates to novel substituted heterocyclic carboxamides, to processes for their preparation, to their use alone or in combinations for the treatment and / or prevention of diseases and to their use for producing medicaments for the treatment and / or prevention of diseases, in particular for the treatment and / or prevention of breathing difficulties including sleep-induced breathing difficulties such as central and obstructive sleep apnoea, snoring (primary and obstructive snoring), dysphagia, peripheral and cardiac vascular disorders including diabetic microangiopathies and disorders of the peripheral and central nervous system including neurodegenerative and neuroinflammatory disorders.

This invention provides a novel GABA structure with better efficacy, reduced side effects, and greater safety for clinical use. A This invention relates to receptor agonists, specifically a phenol derivative, its preparation method, and its use in the central nervous system. The phenol derivative provided by this invention offers more and better drug options for inducing or maintaining anesthesia in animals or humans, promoting sedation and hypnosis, and treating and / or preventing anxiety, nausea, vomiting, migraines, seizures, epilepsy, neurodegenerative diseases, and other central nervous system-related disorders.

Disclosed in the present invention is the use of a mesenchymal-stem-cell-derived intracellular nanovesicle in neuroprotection. Compared to a small extracellular vesicle with exosomes as the main component, the small intracellular nanovesicle of the present invention has a smaller particle size, a narrower particle size distribution range, and greater stability at different temperatures, and has good tissue compatibility. The small intracellular nanovesicle of the present invention can better ameliorate nerve injury or neurodegenerative diseases such as optic nerve injury, ischemic stroke and Alzheimer's disease, and has very good application and research value in the field of pharmaceuticals.

The disclosure provides a method of preventing or reducing protein aggregates using combretastatin-A4 (CA4) or an analog thereof. The disclosure also provides methods of reducing the risk, delaying the onset, delaying or slowing the progression, or reversing the signs or symptoms of a neurodegenerative (or other age-progressive) disease using a combretastatin-A4 (CA4) or an analog thereof. The combretastatin-A4 (CA4) or an analog thereof may bind glial fibrillary acidic protein (GFAP). The combretastatin-A4 (CA4) or an analog thereof is described by compounds of Formula (I).

Disclosed is a method for treating a disease or condition characterized by neurodegeneration by administering to a subject in need thereof a therapeutically effective amount of a compound selected from the group consisting of hinokitiol, a hinokitiol derivative, and an iron-transporting tropolone.

The present invention relates to the use of TDP1 and eltrombopag in the treatment of myotonic dystrophy type 2. The present invention uses a fruit fly model to identify that TDP1 knockdown can effectively rescue neurodegeneration in the CCTG repeat fruit fly model, reduce pigment production block, cell death and ommatidium fusion, and improve motor defects. At the same time, in vitro screening using small molecules found that eltrombopag can be used as a TDP1 inhibitor and can significantly reduce disease cytotoxicity. The present invention provides a new target and pharmacological substance for CCTG repeat expansion diseases in myotonic dystrophy type 2, and expands the medical use of eltrombopag. The present invention provides a new drug with clinical application prospects for the treatment of CCTG repeat expansion diseases in myotonic dystrophy type 2.

The invention relates to application of 1-allyl piperazine or pharmaceutically acceptable salt thereof in preparation of a medicine for treating Parkinson's disease. A caenorhabditis elegans PD model is adopted to prove for the first time that on one hand, 1-allyl piperazine can obviously enhance autophagy activity in a model animal body, efficiently promote removal of aggregation alpha-synuclein and radically relieve damage of Parkinson's disease characteristic pathological protein deposition to neurons, and on the other hand, 1-allyl piperazine can effectively promote removal of aggregation alpha-synuclein and radically relieve damage of Parkinson's disease characteristic pathological protein deposition to neurons. The compound can effectively activate mitochondrial unfolded protein reaction. The autophagy activation pathway and the mitochondrial function regulation pathway can generate a synergistic effect to jointly relieve the neurodegeneration process related to the Parkinson's disease, so that dopaminergic neurons are protected, and the pathological progress of the disease is delayed.

The present application relates to siRNA and oligonucleotide agents for use in the prevention or treatment of SOD1-related neurodegenerative diseases or conditions, such as amyotrophic lateral sclerosis, ALS. The oligonucleotide agent comprises a double-stranded targeting oligonucleotide (siRNA) and a non-targeting single-stranded oligonucleotide (ACO), wherein the siRNA targets the mRNA region of the target gene SOD1.

Disclosed is a method of treating a disease or condition characterized by neurodegeneration via administering to a subject in need thereof a therapeutically effective amount of a compound selected from the group consisting of hinokitiol, hinokitiol derivatives, and iron-transporting tropolones.

Microglial spatial heterogeneity remains a crucial yet poorly studied question in light of potential cell-directed therapies for Alzheimer`s disease (AD). Little is known about the dynamics of spatially distinct microglia states, which are either adjacent or non-associated with the plaque site, and their selective contributions to neurodegeneration in vivo. So far, research has essentially focused on pathology-associated microglia. Here, we combined novel multicolor fluorescence fate mapping, single-cell transcriptional analysis, epigenetic profiling, advanced immunohistochemistry and computational modelling to comprehensively characterize the relation of plaque-associated and non-plaque- associated microglia during neurodegeneration. This approach enabled us to identify and characterize non-plaque-associated microglia as a unique and highly dynamic microglial state in a mouse model of AD. Non-plaque-associated microglia modulate network expansion, quickly adapt to environmental cues and their transition to plaque-associated microglia can be specifically modulated during disease, contrary to their reputation as a passive bystander subpopulation. This description of the dynamics of spatially segregated microglial states and their distinct molecular features may therefore open promising new avenues for state-specific therapeutic interventions during neurodegeneration.

The present disclosure relates to anti-human CD154 antibodies having a modified effector function. The present disclosure also relates to the use of these anti-human CD154 antibodies in the treatment of conditions associated with CD154 activation, the conditions associated with CD154 activation are, for example, transplant rejection, inflammatory conditions and diseases, dysfunctional immune responses associated with viral infections and diseases, autoimmune conditions and diseases, allergic conditions, atherosclerotic conditions, or neurodegenerative conditions and diseases. The present disclosure also relates to the use of these anti-human CD154 antibodies in inducing central tolerance and hematopoietic cell chimerism in transplanted patients.

The present invention relates to a compound of formula (I) or a pharmaceutically acceptable salt and / or solvate thereof. The invention also relates to the use of the compounds of formula (I) as a medicament, in particular for the prevention or treatment of obsessive-compulsive disorder and related behaviors, including addiction, obsessive-compulsive disorder and dietary disorder, and neurodegenerative diseases, such as Parkinson's disease or Alzheimer's disease.

The invention is concerned with a fusion protein comprising interleukin 13 and a regulatory cytokine, for example, an interleukin chosen from interleukin 4, interleukin 10, interleukin 27, interleukin 33, transforming growth factor beta 1, transforming growth factor beta 2, and interleukin 13, a nucleic acid molecule encoding such fusion protein, a vector comprising such nucleic acid molecule, and a host cell comprising such nucleic acid molecule or such vector. The invention further pertains to a method for producing such fusion protein. The fusion protein or a gene therapy vector encoding the fusion protein may be used in the prevention or treatment of a condition characterized by pathological pain, chronic pain, neuro-inflammation and / or or neurodegeneration.

Methods and compositions for diagnosing brain injury, neurodegeneration; or a predisposition thereto, in a subject are provided. Particularly, the present invention relates to specific antigen antibody reactivities useful in diagnosing brain injury, neurodegeneration or a predisposition thereto, in a subject.

Disclosed in the present application are a method and drug for preventing or treating a neurodegenerative disease, whereby a therapeutically effective amount of gliclazide or a pharmaceutically acceptable salt thereof or a combination of gliclazide or a pharmaceutically acceptable salt thereof and acetaminophen or a pharmaceutically acceptable salt thereof is used or comprised. The method and drug of the present invention can significantly alleviate symptoms such as hyposmia, cognitive dysfunction, and psychiatric symptoms in patients with neurodegenerative diseases that cannot be treated with existing drugs, and can be particularly used for controlling the progression of neurodegenerative diseases.

Antisense oligonucleotides are provided which target potassium channel tetramerization domain containing 20 (KCTD20) and can be used in treating, inhibiting, or reducing the severity of a neurodegenerative disease, especially those involving glutamate excitotoxicity.

The present invention relates to compounds of formula (I) for use as neuroprotective agents and / or in inhibiting formation of alpha-synuclein aggregates in vivo. The invention further relates to methods of inhibiting neurodegeneration and / or inhibiting formation of alpha-synuclein aggregates in vivo.

The present disclosure relates to lemborexant, a dual orexin receptor antagonist, and compositions and methods for use in the treatment of Alzheimer's disease (AD), for example, in subjects having or at risk of developing AD. [Solution] A method for treating Alzheimer's disease (AD) in a subject having or at risk of developing AD, comprising administering to the subject a therapeutically effective amount of lemborexant, a pharmaceutically acceptable salt thereof, or a solvate thereof, thereby treating AD.

The invention relates to gene therapy, and more specifically, to AAV gene therapy vectors containing a novel chimeric deoxyribonuclease (DNase) protein transgene and methods of treating ailments such as cancer and neurodegeneration.

Methods and compositions for preventing or treating cognitive decline associated with dementia and / or mild cognitive impairment and / or neurodegeneration using antibodies, peptides, fusion proteins, or genome editing systems that modulate HSPG / heparin binding affinities of ApoE.

The invention relates to an active agent increasing the activity of α-carbonic anhydrase (hCA) enzymes, having the potential for use in the treatment of Alzheimer's and certain neurodegenerative disorders.

Methods and composition are provided for treatment of various disorders associated with decreased neurogenesis, including age-related neurodegeneration, such as Alzheimer' s disease.

Disclosed are compounds, compositions, and methods for inhibiting tyrosine-mediated DNA repair in a neuroprotective manner and / or activating transcription and / or protein synthesis. Compositions include a resveratrol, such as cis-resveratrol, or a compound of Formula I or Formula II. Compounds of Formula I and Formula II have the following structureswhere the variables, e.g., Y1, Y2, Y3, R1, R2, R3 the A-ring, and W are defined herein. Said compound and compositions may be utilized in treating aging and age-associated neurocognitive and metabolic disorders including various types of cancer. In particular, compositions disclosed herein are neuroprotective against tyrosine / phenylalanine or their metabolites-mediated neurodegeneration and neurocognitive disorders. The disclosure also includes combination pharmaceutical compositions and methods of treatment in which cis-resveratrol, a compound of Formula I, a compound of Formula II, or a pharmaceutically acceptable salt thereof is used in combination with a GLP-1 receptor agonist for treating a traumatic brain injury or a neurodegenerative disorder.

The traditional Chinese medicine comprises (1) radix puerariae, (2) radix angelicae sinensis, (3) radix salviae miltiorrhizae, (4) radix codonopsis, (5) radix astragali, (6) fructus perillae, (7) fructus ziziphi jujubae, (8) radix bupleuri, (9) radix scutellariae, (10) flos carthami, (11) radix curcumae, (12) radix et rhizoma rhei, (13) pericarpium zanthoxyli, (14) radix glycyrrhizae, (15) radix ophiopogonis, (16) fructus schizandrae, (17) radix aconiti carmichaeli, (18) radix ginseng, (19) poria cocos, (20) gypsum, (21) oyster, (22) cassia twig and (23) semen plantaginis. Or extracts of the above components, the amount of the extracts being equivalent to the amount of the raw materials of the corresponding components. The invention aims at the clinical curative effect of amyotrophic lateral sclerosis diseases with different pathological manifestations. The medicine can be combined with western medicines for use.

Disclosed herein is a blood-based two-part diagnostic tool designed to diagnose a pre-symptomatic neurodegenerative disease. The first part consists of assays designed for amplifying and sequencing predetermined regions of cell-free DNA. The second part consists of python-derived conduits that analyze methylation characteristics to identify neuronal-derived DNA and provide a diagnosis of a pre-symptomatic neurodegenerative disease.

Methods and compositions that treat Alzheimer's disease and other neurodegenerative diseases and / or to ameliorate or improve symptoms associated with Alzheimer's disease. In some aspects, the compositions and methods use a serotonin 4 receptor (5-hydroxytryptamine (serotonin) receptor 4, or 5-HT4R) agonist in combination with: (R,S)-ketamine, a (R,S)-ketamine analog, or a pharmaceutically acceptable salt, derivative, or metabolite thereof; an antagonist of the glutamate N-methyl-D-aspartate (NMDA) receptor (NMDAR); or an agonist of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR).

Structural design of cranial nerve degeneration contrast agent precursor, the cranial nerve degeneration contrast agent prepared using the cranial nerve degeneration contrast agent precursor can be used for positron radiation tomography to detect alpha-synuclein. Since the cranial nerve degeneration contrast agent has better affinity and specificity for α-synuclein, it is helpful for more efficient early diagnosis of Parkinson's disease.

To provide therapies, methods and uses that overcome the drawbacks of existing therapies of neurodegenerative pathologies.SOLUTION: The present specification discloses modified anti-PD-L1 antibodies that abolish Fc-related effector function and enhance clearance rate while maintaining therapeutic efficacy for neurodegenerative disease modification. The present specification also discloses a nucleic acid sequence and an expression construct encoding the modified anti-PD-L1 antibodies, as well as a method for producing the modified anti-PD-L1 antibodies. In addition, the present specification discloses methods of treatment and uses that employ an administration regime of the disclosed anti-PD-L1 antibodies that ensures the antibodies are present for only a specific period of time and then are sufficiently cleared from the body to ensure treatment efficacy is maintained.SELECTED DRAWING: Figure 32