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163
resultados
Última actualización
20/03/2026 [07:34:00]
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: 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: 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: 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: 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: 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: 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: 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: 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: EP4706644A1
The present invention relates to: reconstituted high-density lipoprotein nanoparticles comprising cholesterol; and a composition for preventing or treating Alzheimer's disease and cancer, the composition comprising the nanoparticles. Specifically, the reconstituted high-density lipoprotein nanoparticles comprising cholesterol according to the present invention have an excellent cell influx rate and promote cholesterol efflux from cells, thus having a cancer cell killing effect, and can therefore be used for preventing or treating cancer.
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: 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.
Resumen de: GB2700773A
A compound of formula (I) or a pharmaceutically acceptable salt thereof: wherein Ring A is selected from: R1 is: halo, -CN, C1-C6 alkyl, C1-C6 haloalkyl, C3-C6 cycloalkyl, -O-C1-C6 alkyl or -SO2-C1-C6 alkyl; R2 is: H, halo, or -CN; R3, R5, and R6 are each independently: H, halo, or -O-C1-C6 alkyl; R4 is independently: halo, -CN, C1-C6 alkyl, -O-C1-C6 alkyl, C3-C6 cycloalkyl, -O-C3-C6 cycloalkyl, or -O-C1-C6 alkyl-C3-C6 cycloalkyl; wherein said C1-C6 alkyl, -O-C1-C6 alkyl, C3-C6 cycloalkyl, -O-C3-C6 cycloalkyl, and -O-C1-C6 alkyl-C3-C6 cycloalkyl, are optionally substituted with from 1 to 6 groups each independently: deuterium, -CN, halo, -O-C1-C3 alkyl, or -O-C1-C3 haloalkyl; R7 is halo, or -O-C1-C6 alkyl; X1 is CR8; and R8 is H, halo, C1-C6 alkyl, C1-C6 haloalkyl, -O-C1-C6 alkyl, or -O-C1-C6 haloalkyl. The compounds are GPR17 modulators. Also disclosed are pharmaceutical compositions comprising the compounds; and the compounds for use in the treatment of diseases and conditions associated with GPR17, including multiple sclerosis, amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD). Figure formula (I)
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.
Resumen de: AU2026201203A1
Compounds described herein may be used for the treatment of neurodegenerative diseases linked to protein misfolding, including prion diseases, Alzheimers' disease, Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), and also other neurodegenerative, degenerative, metabolic and ischemic conditions. Indeed, NAD metabolism impairment is also a critical feature in brain ischemia/reperfusion injury, Wallerian degeneration, kidney failure, multiple sclerosis, aging, and metabolic disorders such as diabetes mellitus. Therapies that elevate or stabilize NAD levels may thus have broad potential for treating many severely debilitating neurological and metabolic conditions. Evidence is provided herein with compounds from 8 lead series for NAD restoring properties and for therapeutic efficacy in cellular and/or animal models of prion disease, PD and ALS. eb e b
Resumen de: AU2024345495A1
The disclosure pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, the disclosure describes methods of assaying a sample obtained from a subject having or suspected of having a cognitive impairment for one or more proteins selected from: DLL1, VNN2, VAV3, and SUMF1. In certain embodiments, the cognitive impairment is caused by a neurodegenerative disease, such as Alzheimer's disease. The methods further comprise identifying a subject as likely or not likely to respond positively to the plasma exchange therapy. In even further aspects, the disclosure describes methods for treating a cognitive impairment in the subject by a plasma exchange therapy, wherein based on the specific protein expression data, the subject is identified as likely or not likely to respond positively to the plasma exchange therapy. The plasma exchange therapy can be full and/or low volume plasma exchange. Also provided are kits suitable for performing the methods disclosed herein.
Resumen de: AU2024327965A1
Material compositions and/or methods useful for the prophylaxis and/or treatment of a-syn protein depletion (proteinopenia) are provided, including material compositions that retain native function of a-syn protein while limiting and/or preventing amyloid formation and/or aggregation of said protein. Material compositions and formulations for enhancing protein solubility, stability, circulation time, receptor interaction, brain penetrance, CSF halflife, and for facilitating peptide/protein synthesis and purification are also provided.
Resumen de: WO2026047040A1
The present invention relates to a compound of formula (I) wherein R1 is a hydrogen atom, halogen or -(C1-C2)alkyl, R2 is -halo(C1-C2)alkoxy, and R3 and R4 form together with N to which they are attached an optionally substituted 5-7 membered monocyclic heterocycloalkyl ring or an optionally substituted 8-11 membered bicyclic heterocycloalkyl ring. The present invention also relates to a medicament and a pharmaceutical composition comprising said compound of formula (I), as well as their therapeutic uses, in particular as inhibitor of NOD-like receptor protein 3 inflammasome for preventing and/or treating Parkinson's disease, frontotemporal Dementia, Multiple System Atrophy, Alzheimer's disease, Multiple Sclerosis, Amyotrophic Lateral Sclerosis or brain injury.
Resumen de: US20260061011A1
A Bifidobacterium animalis subsp. lactis for reducing Abeta42 deposition and an application, a name of the Bifidobacterium animalis subsp. lactis is Bifidobacterium animalis subsp. lactis IOB-LO7, and classified as Bifidobacterium animalis subsp. lactis, the Bifidobacterium animalis subsp. lactis IOB-LO7 is preserved in the General Microbiology Center of the China General Microbiological Culture Collection Center (CGMCC) on Dec. 23, 2021, with the collection number of CGMCC No. 24185. By reducing the levels of Aβ42 in the cerebral cortex and hippocampus, clearing Aβ amyloid plaques, improving communication between neurons, reducing brain neuroinflammation, and protecting nerve cells, it helps to restore cognitive function and improve Alzheimer's disease. Additionally, it can also improve gut microbiota imbalance caused by Alzheimer's disease.
Resumen de: US20260062497A1
Provided are pharmaceutical formulations and dosing regimen for antibody-based treatment of amyotrophic lateral sclerosis (ALS).
Nº publicación: US20260060947A1 05/03/2026
Solicitante:
INST PASTEUR DE MONTEVIDEO [UY]
UNIV DE LA REPUBLICA [UY]
INSTITUT PASTEUR DE MONTEVIDEO,
UNIVERSIDAD DE LA REP\u00DABLICA
Resumen de: US20260060947A1
This invention relates to the use of nitroalkene derivatives for the treatment of neurodegenerative conditions in mammals in which neuroinflammation is a contributing factor, such as in amyotrophic lateral sclerosis (ALS).
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