Resumen de: US20260284230A1
0000 Provided herein are compositions and methods of treating and/or preventing amyotrophic lateral sclerosis (ALS) in a subject in need thereof, the methods comprising administering an agent wherein the agent modifies neurons via changes in Kcnn1 protein expression or activity, which in turn modifies neuron firing and/or increases the clearance or protection from toxicity of an ALS-causing protein.
Resumen de: US20260284097A1
0000 The disclosure relates to double stranded ribonucleic acid (dsRNAi) agents and compositions targeting the APP gene, as well as methods of inhibiting expression of an APP gene and methods of treating subjects having an APP-associated disease or disorder, such as Alzheimer's disease (e.g., early onset Alzheimer's disease), using such dsRNAi agents and compositions.
Resumen de: DE102025111075A1
Die vorliegende Erfindung betrifft ein Verfahren zur Herstellung von dopaminergen neuronalen Organoiden (d-NOs) mit Nachweis der Dopaminfreisetzung in biologisch wirksamen Konzentrationen. Darüber hinaus umfassen d-NOs neben dopaminergen Neuronen auch funktionell miteinander verbundene GABAerge, glutamaterge und cholinerge Neuronen sowie Gliazellen, wodurch sie zu einem multizellulären Organoid mit einer für das Mittelhirn repräsentativen Zellzusammensetzung und Funktion werden. Daher zeigen die d-NOs der Erfindung eine komplexe Regulation dopaminerger Neuronen durch verwandte exzitatorische und inhibitorische Neuronen, was auf Kontrollmechanismen hindeutet, die beispielsweise eine Überproduktion und Freisetzung von Dopamin verhindern können. Die Erfindung bezieht sich auch auf die n-NOs als Implantat oder zur Verwendung bei der Behandlung der Parkinson-Krankheit. Darüber hinaus bezieht sich die Erfindung auf die Verwendung der d-NOs für Wirkstoffscreenings.
Resumen de: WO2026198526A1
The present disclosure provides compositions and methods for treating a subject afflicted with or at risk of developing a neurological condition, including a synucleinopathy such as Parkinson's disease, increasing mitochondrial function, reducing alpha-synuclein aggregation, and decreasing cellular oxidative stress. Aspects of the disclosure further relate to molybdenum diselenide nanomaterial compositions and combinatorial therapies for neuroprotection.
Resumen de: WO2026198539A1
The present disclosure provides products and methods for modulating brain lipid function and dysfunction in a subject. In some aspects the methods are useful for slowing the progression of or preventing the development of Alzheimer's Disease or for treating Alzheimer's disease. The disclosure provides the results of a genome-wide CRISPR screening to reveal regulators of oligodendrocyte lipid dysfunction.
Resumen de: WO2026193686A1
The present invention belongs to the technical field of biopharmaceutics, and specifically relates to a pharmaceutical composition for preventing and/or treating Alzheimer's disease. Provided in the present invention is an NPAFP protein-based pharmaceutical composition. The composition exhibits significant effects in anti-oxidation, improving mitochondrial quality, reducing the secretion of Aβ42, ameliorating the pathological state caused by Tau PFF, etc., thereby providing a new idea for the prevention and treatment of Alzheimer's disease.
Resumen de: US20260284041A1
0000 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: WO2026197766A1
The present invention relates to a composition comprising a compound represented by chemical formula 1 for use in preventing, treating, or ameliorating amyotrophic lateral sclerosis (ALS), and a use thereof. The composition of the present invention can exhibit an excellent effect in preventing, treating, or ameliorating amyotrophic lateral sclerosis (ALS) and/or related symptoms.
Resumen de: US20260284153A1
A method for treating periodontal disease, atherosclerosis caused by the periodontal disease, and/or Alzheimer's disease includes administering a composition comprising a peptide having an amino acid sequence of SEQ ID NO: 1 to a subject in need thereof. The composition is effective in suppressing osteoclastogenesis, suppressing Porphyromonas gingivalis colony formation, and suppressing gingipain expression. Further, the composition is safe to a living body and involves less side effects including abnormal response.
Resumen de: US20260284023A1
Methods of use of CFTR corrector compounds, particularly lumacaftor and tezacaftor, to treat reduced cerebral perfusion associated with heart failure, sudden sensoneurinal hearing loss, vascular dementia, arterial hypertension, ischemic stroke, hemorrhagic stroke, heart disease, diabetes and Alzheimer's disease by treatment with an amount sufficient to provide a proteostatic effect on cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in cerebral artery smooth muscle cells and an increase in cerebrovascular perfusion in the patient.
Resumen de: AU2025235730A1
The present disclosure is generally directed to tetracyclic analogs that modulate autophagy in a subject suffering from alpha-1 antitrypsin deficiency (ATD) and possibly other autophagy associated diseases or disorders, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis.
Resumen de: WO2025104230A1
The present disclosure relates to compounds that are IL-17A modulators. The compounds have the structural Formula I defined herein. The present disclosure also relates to processes for the preparation of these compounds, to pharmaceutical compositions comprising them, and to their use in the treatment of diseases or disorders associated with modulation of IL-17A activity.
Resumen de: MX2026005980A
The invention provides compositions and methods for the treatment of diseases associated with amyloid deposits of Aβ in the brain of a patient, such as Alzheimer's Disease. Such methods entail administering a pharmaceutical composition comprising an immunogenic fragment of Aβ capable of inducing a beneficial immune response in the form of antibodies to Aβ. The immunogenic fragments comprise linear or multivalent peptides of Aβ. Pharmaceutical compositions comprise the immunogenic fragment chemically linked to a carrier molecule which may be administered with an adjuvant.
Resumen de: EP4810493A1
The present invention relates to a heterocyclic carbonyl derivative modulator, a preparation method therefor, and the use thereof. Specifically, the present invention relates to a compound represented by general formula (II-B), a preparation method therefor, a pharmaceutical composition containing said compound, and a use thereof as a modulator in the treatment of Alzheimer's disease, schizophrenia, pain, addiction, and sleep disorders, wherein each substituent in general formula (II-B) is as defined in the description.
Resumen de: US20250152747A1
0000 Provided herein are expression cassettes for expressing a transgene in a cell, wherein the transgene encodes a GCase polypeptide. Also provided are methods to treat Gaucher Disease or GBA-PD. Further provided herein are vectors (e.g., rAAV vectors), viral particles, pharmaceutical compositions, and kits for expressing an GCase polypeptide in an individual in need thereof.
Resumen de: US20260275314A1
The disclosure relates to compositions and methods for, inter alia, altering, e.g., enhancing, the level of GBA1 protein via delivery using an adeno-associated viral (AAV) capsid variant. The compositions and methods of the present disclosure are useful, inter alia, in the treatment of subjects who have, have been diagnosed with, or are at risk of having a GBA1-related disorder, e.g., Parkinson's Disease (PD), Gaucher Disease (GD), Parkinson's Disease Dementia (PDD), Dementia with Lewy Bodies (DLB), or Lewy Body Dementia (LBD).
Resumen de: US20260275352A1
The present disclosure relates to AAVs encoding a SOD1 targeting polynucleotide which may be used to treat amyotrophic lateral sclerosis (ALS) and delivery methods for the treatment of spinal cord related disorders including ALS.
Resumen de: WO2026192853A1
The present disclosure provides pharmaceutical compositions and methods for the treatment, delaying progression and prevention of degenerative cognitive disorders such as Alzheimer's disease (AD) and its variations. There are also provided methods of treating AD in human subject by reducing amyloid pathology and improving synaptic integrity.
Resumen de: WO2026190230A1
The present invention relates to alpha-synuclein antibodies which are useful in diagnostic assays for detecting aggregates, oligomers and fibrillar forms of alpha- synuclein in patient samples. These antibodies enable diagnosis and efficient treatment of alpha-synucleinopathies such as Parkinson's Disease (PD) or Multiple System Atrophy (MSA) patients by assessing and monitoring the pathological alpha-synuclein levels in patients.
Resumen de: US20260274931A1
Disclosed herein are methods of conducting clinical trials in Alzheimer's disease (AD). Methods of selecting a medicament and treating an AD subject are disclosed. Methods, systems, kits, and devices for selecting a subject in AD clinical trials and treatment protocols are disclosed herein.
Resumen de: US20260275333A1
Disclosed herein are oligonucleotides with one or more spacers or without a spacer. In various embodiments, STMN2, KCNQ2, UNC13A, or SMN2 oligonucleotides with spacer(s) reduce STMN2 transcripts with cryptic exons or reduce mis-spliced KCNQ2, UNC13A, or SMN2 transcripts and increase full length STMN2, KCNQ2, UNC13A, SMN transcripts, thereby imparting therapeutic efficacy against neurological diseases such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Alzheimer's disease (AD) or spinal muscular atrophy (SMA).
Resumen de: WO2026193281A1
Provided herein are compositions and methods for reducing expression of RBM39 and for treating diseases and/or conditions characterized by increased expression of RBM39 (e.g., a cancer) in subjects in need thereof, by administering compositions comprising compounds described herein. Also provided herein are compositions and methods for reducing expression of MSH3 and for treating diseases and/or conditions characterized by increased expression of MSH3 (e.g., Huntington's Disease) in subjects in need thereof, by administering compositions comprising compounds described herein.
Resumen de: WO2026193123A1
The present disclosure provides combinations of anti-CD3 antibodies (e.g. Foralumab), anti-amyloid therapies, and anti-tau therapies for the treatment of Alzheimer's disease.
Resumen de: US20260272856A1
This disclosure relates to administration of a combination of: 1) about 100-110 mg, about 104-106 mg, or about 105 mg or less of bupropion hydrochloride, or a molar equivalent amount of the free base form or another salt form of bupropion; and 2) about 40-50 mg, about 44-46 mg, or about 45 mg or less of dextromethorphan hydrobromide, or a molar equivalent amount of the free base form or another salt form of dextromethorphan in human patients for treating neurological and psychiatric conditions, such as agitation associated Alzheimer's disease and/or reducing relapse of agitation in Alzheimer's disease.
Nº publicación: WO2026188369A1 17/09/2026
Solicitante:
HIGENE HANGZHOU BIOTECHNOLOGY CO LTD [CN]
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Resumen de: WO2026188369A1
The present invention belongs to the technical field of biopharmaceuticals and specifically relates to use of a pharmaceutical composition in the preparation of a formulation for treating Parkinson's syndrome. Research has found that NPAFP1, NPAFP4, and NPAFP12 proteins can ameliorate the pathological features of a PD model by increasing the fluidity of α-synuclein.