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170
resultados
Última actualización
22/03/2026 [07:55:00]
Resumen de: WO2026056131A1
The use of a TRPM7 activator in preparing a therapeutic product for treating Alzheimer's disease is provided. The TRPM7 activator can be a regulator of an extracellular divalent cation or a metal salt containing a divalent cation. The TRPM7 activator can retain memory and cognitive functions, protect synaptic density and reduce Aβ plaque accumulation in a mouse model of Alzheimer's disease, and the morphology and organ weight analysis of heart, liver and pancreas show that the administration of the TRPM7 activator is safe. In addition, a TRPM7 gene or a protein encoded by the TRPM7 gene can serve as a therapeutic target for treating Alzheimer's disease. A high throughput method for screening potential drug targets for treating Alzheimer's disease by screening TRPM7 activators via TRPM7 proteins broadens idea and provides a new direction for discovery and development of new agents for treating Alzheimer's disease.
Resumen de: WO2026057822A1
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.
Resumen de: WO2026055750A1
The present disclosure relates to the field of oligonucleotides. More particularly, the present disclosure relates to antisense oligonucleotides for the specific binding and inhibition of translation of Chitinase (CHIT1) encoding mRNA. Additionally, this disclosure relates to methods of using such oligonucleotides in preventing or treating diseases, disorders or conditions associated with CHIT1, such as neurodegenerative or neuroinflammatory diseases, disorders or conditions like ALS.
Resumen de: WO2026056971A1
Provided in the present invention is an anti-prothrombin/phosphatidylserine antibody, comprising a heavy chain variable region and a light chain variable region; the heavy chain variable region comprises HCDR1 to HCDR3 having amino acid sequences as shown in SEQ ID NOs: 1-3, respectively, and the light chain variable region comprises LCDR1 to LCDR3 having amino acid sequences as shown in SEQ ID NOs: 4-6, respectively. The anti-prothrombin/phosphatidylserine antibody of the present invention can bind to a prothrombin/phosphatidylserine complex with high affinity, thereby targeting and binding to phosphatidylserine, and has a potential therapeutic effect with respect to tumors, infections, atherosclerosis, ischemia-reperfusion injury, inflammatory bowel disease, Alzheimer's disease, Parkinson's disease, etc.
Resumen de: WO2026057634A1
The present disclosure relates to a compound of formula (I) which is in crystalline Form 1, characterized by having a powder X-ray diffractogram displaying peaks expressed as degree 2-Theta angles at about 3.3, 10.0, 20.1, 21.7, and 25.0. The present disclosure also relates to processes for its preparation, as well as a medicament and a pharmaceutical composition comprising it. The present disclosure further concerns the crystalline Form 1 of compound of formula (I) for use as a medicine and more particularly in the prevention and/or in the treatment of Parkinson's disease, frontotemporal dementia, multiple system atrophy, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, or brain injury.
Resumen de: US20260076927A1
The present invention features palatable pharmaceutical compositions including sodium phenylbutyrate and methods for the treatment of inborn errors of metabolism (e.g., Maple Syrup Urine Disease or Urea Cycle Disorders), neurodegenerative disorders such as Parkinson's disease, spinal muscular atrophy, dystonia, or inclusion-body myositis with such compositions.
Resumen de: WO2026059890A1
The present invention is directed to a pharmaceutical composition and method for treating a subj ect diagnosed amyotrophic lateral sclerosis (ALS) with a pharmaceutical composition containing dissolved or dispersed therein a SOD1 and/or TDP-43 aggregation- inhibiting amount of a rose bengal (RB) compound that is a pharmaceutically acceptable salt of RB, RB lactone, a RB amide, an aromatic RB derivative, wherein the aromatic derivative is an ester or amide formed from an alcohol or monosubstituted amine having a 5 - or 6 -membered aromatic ring, or a 5, 6 - or 6, 6 - fused aromatic ring system that contains 0, 1, or 2 hetero ring atoms that are independently nitrogen, oxygen or sulfur. This treatment method is typically repeated a plurality of times or until the subj ect no longer needs it.
Resumen de: US20260076939A1
The present invention relates to: a method for preparing a chiral gamma lactam derivative or a pharmaceutically acceptable salt thereof by using a chiral organocatalytic compound; and a composition for preventing, alleviating or treating muscle diseases, mental diseases, or neurodegenerative diseases, comprising the derivative or the pharmaceutically acceptable salt thereof. The chiral gamma lactam derivative or the pharmaceutically acceptable salt thereof, of the present invention, has an effect of inhibiting MAO-B and MSTN, targets D1-mClu5, and can be used in the prevention, alleviation, or treatment of muscle diseases including sarcopenia, mental diseases including depression, neurodegenerative diseases including Parkinson's disease, and the like.
Resumen de: US20260076931A1
The present invention generally provides methods and compositions for the treatment of Parkinson's disease and depression and/or anxiety. The invention relates to recombinant microorganisms, particularly gut-colonizing probiotics, modified to produce L-DOPA.
Resumen de: EP4710934A1
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.
Resumen de: CN121285374A
The present invention provides a method of treating a patient suffering from Parkinson's disease (PD) associated with wild type LRRK2, and a method of treating a patient suffering from Parkinson's disease (PD) associated with wild type LRRK2. The present invention recognizes that the analysis of genetic modification factors of LRRK2 in such patients allows for the identification of patients who will respond to LRRK2 inhibitors. Accordingly, the invention provides methods of identifying PD patients who will respond to LRRK2 inhibitors and methods of treating such patients.
Resumen de: WO2024233788A2
Described herein, inter alia, are compositions and methods of use (e.g., treating Parkinson's Disease and/or reducing the immune response due to needle trauma during cell transplantation) for administering a population of regulatory T (TREG) cells and/or a population of midbrain dopamine (mDA) cells to the brain of a subject.
Resumen de: AU2024334698A1
Provided is an antibody that binds to β-amyloid (Aβ), or an antigen-binding fragment thereof. Further provided are a nucleic acid encoding the antibody or the antigen-binding fragment thereof, a cell comprising the antibody or the antigen-binding fragment or nucleic acid thereof, a pharmaceutical composition, a kit, and the use of the antibody or the antigen-binding fragment thereof in the preparation of a drug used for treating or preventing a disease caused by abnormal accumulation or deposition of Aβ in subjects.
Resumen de: AU2024335242A1
This disclosure relates to methods and compositions for the treatment of Parkinson's disease, a neurodegenerative disorder characterized by a loss of dopaminergic neurons. In particular, this disclosure provides formulations of dopaminergic cells demonstrated to possess a therapeutic impact on both motor and non-motor symptoms of the disease.
Resumen de: WO2026055173A1
The present invention provides a method for identifying a subject having a stabilized circulating peptide. The method comprises detecting the stabilized circulating peptide in a body fluid sample, for example, a serum or plasma sample, from the subject. The method may further comprise treating a neurodegenerative disease, or monitoring or adjusting a treatment of a neurodegenerative disease. Also provided is a kit. The kit comprises a binding protein that specifically binds a stabilized circulating peptide in a body fluid sample, for example, a serum or plasma sample, from a subject. The kit may further comprise an agent for detecting, treating or monitoring a neurodegenerative disease in the subject. The neurodegenerative disease may be Alzheimer disease.
Resumen de: WO2026052795A1
The present invention provides a formulation of metformin and glibenclamide for the prevention and/or treatment of neurodegenerative diseases, preferably chosen among Parkinson's disease, multiple system atrophy, amyotrophic lateral sclerosis, frontotemporal dementia, Lewy body dementia, Huntington's disease and Alzheimer's disease.
Resumen de: US20260071275A1
The present disclosure provides compositions and methods using C9ORF72-mediated genes and expression products thereof for diagnosis, treatment and prevention of amyotrophic lateral sclerosis, frontotemporal dementia, or both, in carriers of a C9ORF72 hexanucleotide expansion. The present invention also relates to a method of identifying therapeutic agents to treat and diagnose amyotrophic lateral sclerosis, frontotemporal dementia, or both, in carriers of a C9ORF72 hexanucleotide expansion based on C9ORF72-mediated genes.
Resumen de: WO2026052700A1
Provided herein is an anti-CD2 antibody or antigen binding fragment thereof for treating and/or preventing ALS in a subject in need thereof.
Resumen de: WO2026055419A1
N-(1,1'-biaryl-4-yl)-N-((1-hydroxycycloalkyl)methyl)-2-(aryl)cyclopropane-1-carboxamide compounds (I) and derivatives are G-protein coupled receptor (GPR) 88 modulators for use in the treatment of a disease mediated by GPR88. Indications include Tourette's Syndrome, Huntington's Disease (HD), Addiction, Parkinson's Disease (PD), Schizophrenia, and Attention Deficit Hyperactivity Disorder (ADHD), choreiform movements, tardive dyskinesia, speech delay, learning disabilities, depression, hyperkinetic movement disorders characterised by chorea and/or dystonia, psychosis, cognitive deficits in schizophrenia, affective disorders, bipolar disorder, Alzheimer's disease, basal ganglia disorders, and tardive dyskinesia.
Resumen de: WO2026055601A1
The invention pertains to a method for reducing amyloid plaques in the brain of a human suffering from a disease characterized by Aβ plaques in the brain. It also concerns the treatment or prevention of diseases characterized by Aβ deposition in the brain, such as Alzheimer's disease, Alzheimer's disease in Down syndrome, and cerebral amyloid angiopathy. Certain aspects of the invention involve methods, doses, or dosing regimens that decrease the risk, frequency, severity, or occurrence of amyloid-related imaging abnormalities (ARIA) in subjects undergoing the described treatments. These aspects ensure that while reducing ARIA-related issues, the methods still effectively remove amyloid β plaques from the subject's brain. Additionally, the methods, doses, or dosing regimens disclosed herein aim to reduce ARIA risks, frequency, severity, or events, in human subjects with one or two alleles of APOE4.
Resumen de: US20260072043A1
The present disclosure provides methods for diagnosing or determining susceptibility to Alzheimer's Disease a subject by obtaining a biological sample from the subject; detecting one or more biomarkers in the biological sample selected from the group consisting of: inflammation biomarkers, oxidative stress biomarkers, insulin resistance biomarkers, and autophagy biomarkers; and diagnosing the subject with Alzheimer's Disease where one or more of the biomarkers is detected in the biological sample. Also provided are methods of treating a subject with Alzheimer's Disease comprising administering to the subject an effective amount of one or more agents for the treatment of inflammation, oxidative stress, insulin resistance, and/or autophagy.
Resumen de: WO2026052031A1
The present invention belongs to the technical field of medicine. Disclosed are a pyranocarbazole derivative and a preparation method therefor, and a pharmaceutical composition thereof and the use thereof. Specifically, disclosed in the present invention are pyranocarbazole derivatives as represented by general formulas I and II. The derivative is prepared by means of artificial synthesis. Further disclosed are a pharmaceutical composition containing the derivative, and the use thereof in resisting inflammation, resisting ischemic cerebral injury, relieving pain, resisting brain trauma, treating post-stroke depression, treating vascular dementia and cerebral small vessel disease, resisting Alzheimer's disease, and treating amyotrophic lateral sclerosis.
Resumen de: EP4706655A1
The purpose of the present invention is to provide a medicinal agent that exhibits the effect of inhibiting aggregation of a causative protein of an HRE-related neurodegenerative disease such as ALS. According to the present invention, rifampicin or a rifampicin compound selected from the group consisting of rifampicin, a derivative thereof, and a salt of rifampicin or the derivative and/or resveratrol or a resveratrol compound selected from the group consisting of resveratrol and a derivative thereof is an active ingredient of a preventive or therapeutic agent for a neurodegenerative disease caused by TDP-43 accumulation, or an active ingredient of a preventive or therapeutic agent for ALS.
Resumen de: EP4707410A2
Disclosed herein are methods and compositions that can be used to improve motor deficits and neuroinflammation in subjects in need, for example subjects suffering from neurodegenerative disorders (e.g., Parkinson's disease). Also disclosed are methods and compositions that can be used to diagnose neurodegenerative disorders, such as Parkinson's disease.
Nº publicación: EP4704821A2 11/03/2026
Solicitante:
KNEPPER PAUL A [US]
Knepper, Paul A
Resumen de: WO2024229414A2
Neurodegenerative diseases are treated by the co-administration to a subject of an effective amount of a stilbene, a flavonol, and a TLR4/MD2 receptor antagonist. A preferred stilbene is resveratrol, a preferred flavonol is quercetin, and a preferred TLR4/MD2 receptor antagonist is curcumin.
BOPI
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