198 results about "Neurodegeneration" patented technology

The invention discloses an anti-neurodegeneration exosome composition as well as a preparation method and application thereof. The anti-neurodegeneration exosome composition is prepared from the following components in parts by mass: 5 to 25 parts of human exfoliated deciduous tooth stem cell exosome, 25 to 85 parts of plant-derived exosome-like nano-vesicles, 12 to 10 parts of ginsenoside Rg, 2 to 10 parts of curcumin and 10 to 20 parts of auxiliary materials. The anti-neurodegeneration exosome composition contains a large amount of cell factors, growth factors, miRNA, mRNAs and other components, is easy to fuse with cell membranes of intestinal epithelial cells, can selectively deliver bioactive substances to recipient cells through a blood-brain barrier, carries out information transmission among different cells, regulates signal transduction among the cells, and has a good anti-neurodegeneration effect. The effects of resisting oxidation, resisting inflammation, resisting aging and the like are achieved.

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.

The present disclosure discusses systems and methods for identifying biomarkers that can help with the diagnosis, prognosis, and treatment choices of patients with neurodegenerative diseases. Diffusion based magnetic resonance imaging can often fail for patients with a neurodegenerative disease because parameters fractional anisotropy, mean diffusivity, and radial diffusivity are based on simple models that can fail in the presence of neurodegeneration, such as demyelination. The present disclosure discusses systems and methods that enhance dMRI images and enable tractography to be performed on images of a damaged nervous system. The damaged tracks identified by the present system can be used as a biomarker for the assessment of patients. In some implementations, the biomarkers are converted into clinical scales that can be used to compare patients to one another or over time.

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.

To provide compositions and methods for treating a disease or condition associated with opening of Cx43 hemichannels in astrocytes or osteocytes, preferably for treating an inflammatory disease or condition or a neurodegenerative disease such as spinal cord injury.SOLUTION: Provided herein are compositions and methods for treating a disease or condition associated with opening (e.g., excessive or prolonged opening) of Cx43 hemichannels, such as inflammatory diseases or conditions and neurodegenerative diseases, e.g., spinal cord injury, Alzheimer's disease, osteoarthritis.SELECTED DRAWING: None

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.

Methods for treating a neurodegenerative disease in a subject in need of treatment thereof comprising restoring TDP-43 function in neurons of the subject. The restoring of TDP-43 function includes repairing nuclear pore complex (NPC) injury, which can include increasing expression of nucleoporin POM121.

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 present invention addresses the problem of providing a pharmaceutical composition, in particular, a compound suitable for the prevention and / or treatment of inflammatory diseases and / or neurodegenerative diseases. The present inventors have completed the present invention by deeply studying the exploration of a compound having an NLRP3 inflammasome activation inhibitory effect and finding that a contracted ring pyridazine derivative has an NLRP3 inflammasome activation inhibitory effect. The contracted pyridazine derivative of the present invention is expected to be used as a prophylactic and / or therapeutic agent for inflammatory diseases and / or neurodegenerative diseases.

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.

A bead-based assay system and methods for screening molecule inhibitors of protein-glycan interactions. The assay system includes at least one donor bead and at least one acceptor bead. A first molecule is coupled to the at least one donor bead. The first molecule comprises a protein. A second molecule is coupled to the at least one acceptor bead. The second molecule comprises a glycan. The bead-based assay system includes a screening molecule to be screened for inhibiting protein-glycan interactions. The screening molecule is enabled to interact at a protein-glycan interface of the first molecule and the second molecule.

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