Resumen de: WO2026030341A1
The present disclosure provides a method of treating or inducing cognitive preservation in a patient with Alzheimer's disease, comprising administering an effective amount of CT1812. The effective amount of CT1812 is 100 mg or 300 mg administered orally once daily. The method demonstrates improvements in cognitive outcomes compared to placebo across multiple measures including ADAS-Cog11, MMSE, ADCS-ADL, and ADCS-CGIC. The method demonstrates improvements in cognitive outcomes in patients with low plasma levels of phosphorylated tau 217 prior to administration.
Resumen de: WO2026030249A1
Described herein is an active Alzheimer's Disease (AD) immunotherapy based on a nanoparticle vaccine comprising a plurality of Aβ peptides and/or a plurality of tau peptides. These peptides may correspond to both soluble and aggregated targets and are displayed on the surface of immunogenic liposomes in an orientation that maintains reactivity with epitope-specific monoclonal antibodies. Also provided are methods of making and using same.
Resumen de: WO2026030596A1
The present disclosure provides recombinantly manufactured fusion proteins comprising a HERV-K (HML-2) Env protein fragment or an analog thereof linked to a human Fc fragment. Embodiments include the administration of the fusion proteins to patients having a disease or a disorder with the intention of mitigating and/or reducing the duration of symptoms associated with the condition or disease (for example but not limited to muscular weakness, paralysis and respiratory failure), and/or preventing symptoms associated with the condition or disease, for example, by preventing motor neuron degeneration and cell death in ALS patients associated with the condition or disease. Accordingly, "treatment" generally means both therapeutic treatment and prophylactic or preventative measures. Improvement after treatment may be manifested as a decrease or elimination of such symptoms, e.g., by a decrease or elimination of symptoms associated with ALS, and/or by a decrease in the duration of such symptoms.
Resumen de: EP4686476A1
The invention refers to the field of neurodegenerative diseases including Alzheimer's Disease and a treatment thereof with a Benzoxazepine compound. Benzoxazepine compounds are e.g. known in the treatment of breast cancer and according to the use of the invention are a first therapeutic and prophylactic treatment for neurodegenerative diseases, including Alzheimer's Disease.The invention further relates to test systems for identifying, mapping, elaborating and evaluating said and further therapeutic and prophylactic uses of compounds of interest and/or other pharmaceutical compositions for the treatment of neurodegenerative diseases, including Alzheimer's Disease. (AD)
Resumen de: NZ812405A
A levodopa derivative including a compound or pharmaceutically acceptable salt, hydrate, and/or solvate thereof, wherein the compound includes substituents which, in aggregate, contain at least 6 carbon atoms which are only bonded to either other carbon atoms or to hydrogen atoms. The levodopa derivative may be formulated as a composition including one or more pharmaceutically acceptable carriers or excipients. The levodopa derivative may be part of a pharmaceutical composition including micro or nano particles in which the levodopa derivative is encapsulated in the pharmaceutically acceptable polymer. The levodopa derivative can be used to treat Parkinson’s disease by administering to a mammal an amount sufficient to treat Parkinson’s disease.
Resumen de: AU2024307361A1
Described herein are crystalline forms of 6-(6-(((1R,2R,3S,5S)-2-fluoro-9-azabicyclo3.3.1nonan-3-yl)(methyl)amino)pyridazin-3-yl)-2-methylbenzodoxazol-5-ol (compound A), a small molecule splicing modulator (SMSM) of mRNA, such as pre-mRNA, encoded by genes, for the treatment of Huntington's disease.
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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: US20260027234A1
The present disclosure provides recombinant vectors encoding a choline acetyltransferase (ChAT) polypeptide, compositions thereof, and methods of use 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: 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: 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.
Nº publicación: WO2026024121A1 29/01/2026
Solicitante:
YUHAN CORP [KR]
YUHAN CORPORATION
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.