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138
resultados
Última actualización
04/02/2026 [07:45:00]
Resumen de: NZ758484A
The present disclosure relates to novel compounds, pharmaceutical compositions containing the compounds and methods of using the compounds and pharmaceutical compositions for treating neurodegerative diseases, including Alzheimer’s disease and cognitive decline. Methods for inhibiting synapse number decline or membrane trafficking abnormalities associated with exposure of a neuronal cell to Abeta species are also disclosed.
Resumen de: NZ799802A
The present disclosure relates to novel compounds, pharmaceutical compositions containing the compounds and methods of using the compounds and pharmaceutical compositions for treating neurodegerative diseases, including Alzheimer’s disease and cognitive decline. Methods for inhibiting synapse number decline or membrane trafficking abnormalities associated with exposure of a neuronal cell to Abeta species are also disclosed.
Resumen de: NZ792513A
Aspects of the disclosure relate to compositions and methods useful for treating Huntington’s disease. In particular, the disclosure provides interfering nucleic acids (e.g., artificial mature miRNAs flanked by a miR-155 or a miR-30 backbone sequence) targeting the huntingtin gene (HTT) and methods of treating Huntington’s disease using the same.
Resumen de: US20260029411A1
The invention provides methods and compositions for accurate identification and determination of Parkinson's disease ante-mortem tissue samples. The determination of Parkinson's disease is based on the binding of localized phosphorylated alpha-synuclein with the nerve feature. The methods disclosed in the invention may be used on myriad tissue types and could be manual or automated.
Resumen de: WO2026021131A1
Disclosed are an aromatic alkylamine ferroptosis inhibitor based on a butylphthalide structure, a preparation method therefor, and an application thereof. The chemical structural formula of the ferroptosis inhibitor is as shown in formula (1) or formula (2). The ferroptosis inhibitor is capable of inhibiting ferroptosis caused by a ferroptosis inducer, and reduces the level of intracellular reactive oxygen species. The ferroptosis inhibitor reduces neurological damage caused by cerebral ischemia-reperfusion, and alleviates symptoms of neurological disorders such as Alzheimer's disease and Parkinson's disease. Compared to the ferroptosis inhibitor Ferrostatin-1, the arylalkylamine compound exhibits better metabolic stability and is suitable for in-vivo efficacy evaluation. Therefore, the novel arylalkylamine compound provided by the present invention demonstrates great application value in the treatment of ferroptosis-related neurological disorders.
Resumen de: AU2024288766A1
The invention relates to liposome-encapsulated apomorphine, processes for preparing said liposome-encapsulated apomorphine and to the use of such in the treatment of Parkinson's disease.
Resumen de: AU2025205168A1
An anti-DAT antibody which is formed from a gene comprising SEQ ID No:2 after transcription and translation. The anti-DAT antibody of the present invention can be made into a composition capable of crossing the blood-brain barrier, and specifically binding to dopamine nerve cells, and achieving excellent efficacy in reducing the accumulation of α- syn in the striatum and delaying the course of Parkinson's disease. An anti-DAT antibody which is formed from a gene comprising SEQ ID No:2 after transcription and translation. The anti-DAT antibody of the present invention can be made into a composition capable of crossing the blood-brain barrier, and specifically binding to dopamine nerve cells, and achieving excellent efficacy in reducing the accumulation of - syn in the striatum and delaying the course of Parkinson's disease. ul u l
Resumen de: AU2025205167A1
A targeting vehicles comprises an extracellular vesicle with a dopamine transporter antibody on a transmembrane protein of the extracellular vesicle, the extracellular vesicle is secreted by a cell transfected with a vector gene, and at least a portion of the vector gene comprises SEQ ID No: 1. The targeting vehicles provided in the present invention can be loaded with drugs and cross the blood-brain barrier to achieve specific binding to dopamine neuron, and regulate the secretion of Parkinson's disease marker proteins and delay the course of Parkinson's disease. A targeting vehicles comprises an extracellular vesicle with a dopamine transporter antibody on a transmembrane protein of the extracellular vesicle, the extracellular vesicle is secreted by a cell transfected with a vector gene, and at least a portion of the vector gene comprises SEQ ID No: 1. The targeting vehicles provided in the present invention can be loaded with drugs and cross the blood-brain barrier to achieve specific binding to dopamine neuron, and regulate the secretion of Parkinson's disease marker proteins and delay the course of Parkinson's disease.20 ul u l
Resumen de: US20260027234A1
The present disclosure provides recombinant vectors encoding a choline acetyltransferase (ChAT) polypeptide, compositions thereof, and methods of use thereof.
Resumen de: WO2026021591A1
The present application relates to a novel micropeptide MP29 and a use thereof and relates to a use of the micropeptide in the preparation of a reagent or drug for preventing, treating, or alleviating diseases related to abnormal mitochondrial energy metabolism in cells, wherein the diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, schizophrenia, aging, photoaging, fatty liver disease, liver fibrosis, liver cirrhosis, liver cancer, diabetic nephropathy, cardiovascular diseases such as heart failure, etc. By means of endogenous overexpression or exogenous synthesis, the reducing equivalents NADH in the tricarboxylic acid cycle are up-regulated to promote intracellular ATP production, thereby significantly enhancing the proliferation of high-energy-demanding cardiac cells and brain tissue cells, or suppressing oxidative damage and apoptosis of cells in Alzheimer's disease models and Parkinsonism, or alleviating hypertrophy and aging of myocardial cells in heart failure models, or ameliorating the photodamage of cells in photoaging models. These results indicate that the micropeptide MP29 has an application value in preventing or treating diseases related to abnormal mitochondrial energy metabolism.
Resumen de: WO2026024121A1
The present disclosure relates to a bicyclic fused-ring (for example, pteridine, pyridopyrimidine, pyridopyrazine, quinazoline, naphthyridine, or quinoxaline) derivative or a pharmaceutically acceptable salt thereof inducing activation of a triggering receptor expressed on myeloid cells 2 (TREM2), a pharmaceutical composition including the same, and a use thereof. The bicyclic fused-ring derivative or a pharmaceutically acceptable salt thereof may be useful in treatment and prevention of TREM2-mediated neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD), FTLD-like syndrome, Parkinson's disease, Huntington's disease and Nasu-Hakola disease.
Resumen de: WO2026024901A1
The present disclosure provides methods of using a small molecule TREM2 agonist or a pharmaceutically acceptable salt thereof to treat Alzheimer's Disease in a human subject.
Resumen de: WO2026024717A1
Provided herein are methods and compositions for treating neurological diseases (e.g., neurodegenerative disorders (e.g., Alzheimer's disease, Parkinson's disease, dementia, a tauopathy, chronic traumatic encephalopathy (CTE), traumatic brain injury (TBI), mild cognitive impairment); psychiatric disorders (e.g., bipolar disorder, schizophrenia, depression, anxiety, post-traumatic stress disorder, obsessive compulsive disorder); inflammation in the central nervous system) using lithium salts, activators that increase the expression or activity of the RE1 silencing transcription factor (REST), or a combination thereof, or in combination with an additional agent.
Resumen de: US20260027157A1
Methods to alleviate or treat Alzheimer's Disease or a neurological disorder or disorder, or to alleviate the symptoms of each thereof are provided, the methods comprising administering an effective amount of (HSPC) or a population of HSPCs to the subject, that are optionally gene-corrected prior to administration and that will differentiate on healthy microglia cells in the brain. The cells are capable of decreasing amyloid plaques and inflammation.
Resumen de: US20260028347A1
The present description relates to compounds, forms, and pharmaceutical compositions thereof and methods of using such compounds, forms, or compositions thereof for treating or ameliorating Huntington's disease.In particular, the present description relates to substituted bicyclic heterocyclic and heteroaryl compounds of Formula (I), forms and pharmaceutical compositions thereof and methods of using such compounds, forms, or compositions thereof for treating or ameliorating Huntington's disease.
Resumen de: US20260027179A1
Disclosed is a method of treating a neurodegenerative disease such as Parkinson's disease, diffuse Lewy body disease, transitional Lewy body dementia, and multiple system atrophy in a subject. The method comprises administering to the subject a therapeutically effective amount of a peptide comprising an α-synuclein binding domain operably linked to a protein transduction domain and a proteasomal targeting domain, wherein the α-synuclein binding domain is derived from a reversed sequence of β-synuclein. Other methods, as well as uses and compositions, are disclosed.
Resumen de: WO2026025015A1
The present disclosure generally relates to the treatment of subjects having Parkinson's disease or at risk of developing Parkinson's disease by administering a SIM BHLH Transcription Factor 2 (SIM2) agonist to the subject.
Resumen de: WO2026022191A1
The present invention relates to the field of neurodegenerative diseases, in particular Alzheimer's disease. The present invention further relates to fibrillary Apolipoprotein E (ApoE) for use in a method of treatment and/or prevention of a neurodegenerative disease and methods of producing said fibrillary ApoE. Moreover, the present invention relates to an antigen-binding peptide specifically binding to fibrillary ApoE, preferably human ApoE, a method of generating said antigen-binding peptide, and its use in a method of treatment and/or prevention and/or diagnosis of a neurodegenerative disease in a patient in need thereof.
Resumen de: US20260027178A1
The present disclosure generally relates to the treatment of subjects having Parkinson's disease or at risk of developing Parkinson's disease by administering a SIM BHLH Transcription Factor 2 (SIM2) agonist to the subject.
Resumen de: WO2026024812A1
The present disclosure provides substituted 2,3,4,5-tetrahydro-1H-benzo e 1,4 diazepin-l-yl compounds, pharmaceutically acceptable salts thereof, or a pharmaceutical composition thereof, utilized in the manufacture of a medicament for the inhibition of F-ATP hydrolase and for treating diseases, disorders or conditions associated with F-ATP hydrolase, including Alzheimer's disease, Parkinson's Disease, amyotrophic lateral sclerosis, Friedreich's ataxia and cancer.
Resumen de: US20260028625A1
The present disclosure relates to an sgRNA and its application in the preparation of a product for the treatment of Huntington's disease. The present disclosure was designed and screened to obtain an sgRNA targeting exon 1 of the human HTT gene as shown in SEQ ID NO: 1 or SEQ ID NO: 2. The CRISPR/Cas9 system mediated HTT gene knockout strategy based on this sgRNA and its high homologue sgRNA can efficiently knock out the human Huntingtin gene and achieve gene therapy for Huntington's disease.
Resumen de: US20260028623A1
Provided are RNAi agents, pharmaceutical compositions, and methods for reducing the amount or activity of PRNP RNA in a cell or a subject, and in certain instances reducing the amount of prion protein in a cell or a subject. Such RNAi agents, pharmaceutical compositions, and methods are useful to ameliorate at least one symptom or hallmark of a neurodegenerative disease. Such neurodegenerative diseases include prion diseases, such as Creutzfeldt-Jakob disease (CJD) (e.g., variant Creutzfeldt-Jakob Disease (vCJD), classic Creutzfeldt-Jakob Disease (cCJD), familial Creutzfeldt-Jakob Disease (fCJD), or sporadic Creutzfeldt-Jakob Disease (sCJD)), Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, or kuru; synucleinopathies such as Alzheimer's disease, Parkinson's disease, or dementia with Lewy bodies; or tauopathies such as frontal temporal dementia associated with a Tau mutation, Pick's disease, progressive supranuclear palsy, corticobasal neurodegeneration, or chronic traumatic encephalopathy (CTE).
Resumen de: AU2024238511A1
The present disclosure relates to biomarkers and uses thereof in methods for selecting a patient diagnosed with amyotrophic lateral sclerosis (ALS) for an ALS therapy. The present disclosure further relates to methods for identifying the severity of ALS in a patient, treating an ALS patient, and monitoring efficacy of an ALS treatment.
Resumen de: EP4685158A1
The present invention relates to the field of neurodegenerative diseases, in particular Alzheimer's disease. The present invention further relates to fibrillary Apolipoprotein E (ApoE) for use in a method of treatment and/or prevention of a neurodegenerative disease and methods of producing said fibrillary ApoE. Moreover, the present invention relates to an antigen-binding peptide specifically binding to fibrillary ApoE, preferably human ApoE, a method of generating said antigen-binding peptide, and its use in a method of treatment and/or prevention and/or diagnosis of a neurodegenerative disease in a patient in need thereof.
Nº publicación: US20260022376A1 22/01/2026
Solicitante:
THE TRUSTEES OF INDIANA UNIV [US]
The Trustees of Indiana University
Resumen de: US20260022376A1
The present disclosure provides novel approaches to the treatment of Alzheimer's disease, and other neurodegenerative disorders such as chronic traumatic encephalopathy (CTE) using novel therapeutics comprising agents that reduce the interaction of a tau seed interactor with intracellular tau proteins and thus reduce or inhibit the production of tau-associated neurofibrillary tangles.
BOPI
Sede Electrónica
