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128
resultados
Última actualización
29/07/2025 [07:29:00]
Resultados 75 a 100 de 128
Resumen de: AU2023403437A1
The present disclosure relates to compositions comprising trehalose and methods of using same for the treatment of Huntington's disease.
Resumen de: US2025195511A1
Novel compounds of Formula (I), and the pharmaceutically acceptable salts thereof, are inhibitors of NLRP3 and may be useful in the treatment, prevention, management, amelioration, control, and suppression of diseases mediated by NLPR3. The compounds of the present invention may be useful in the treatment, prevention or management of diseases, disorders and conditions mediated by NLRP3 such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, osteoarthritis, atherosclerosis, heart failure, idiopathic pericarditis, myocarditis, atopic dermatitis, hidradenitis suppurativa, inflammatory bowel disease, cancer, Alzheimer's Disease, Parkinson's Disease, dementia with Lewy bodies (DLB), and traumatic brain injury.
Resumen de: WO2025125071A1
Cathepsin D peptides are provided that are capable of interacting with and/or inhibiting the formation of beta amyloid aggregates, thereby leading to a competitive reduction of amyloid- amyloid interactions. Also provided are recombinant expression vectors encoding said peptides as well as of pharmaceutical formulations comprising said peptide-analogues. Said peptides, compositions and recombinant vectors are useful as therapeutic agents in the treatment and/or amelioration of the symptoms of amyloidoses such as Alzheimer's disease.
Resumen de: WO2025126158A2
SnRNA systems targeting SOD1 RNA sequences are disclosed herein. Further disclosed are methods of treating Amyotrophic Lateral Sclerosis.
Resumen de: WO2025128777A1
Novel compounds of Formula (I), and the pharmaceutically acceptable salts thereof, are inhibitors of NLRP3 and may be useful in the treatment, prevention, management, amelioration, control, and suppression of diseases mediated by NLPR3. The compounds of the present invention may be useful in the treatment, prevention or management of diseases, disorders and conditions mediated by NLRP3 such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, osteoarthritis, atherosclerosis, heart failure, idiopathic pericarditis, myocarditis, atopic dermatitis, hidradenitis suppurativa, inflammatory bowel disease, cancer, Alzheimer's Disease, Parkinson's Disease, dementia with Lewy bodies (DLB), and traumatic brain injury.
Resumen de: JP2025023319A
To provide compositions and methods for treating and preventing amyotrophic lateral sclerosis.SOLUTION: Dosage regimens for SOD1-targeting antisense oligonucleotides and salts thereof are provided. These dosage regimens find use in the treatment of subjects having or at risk of developing amyotrophic lateral sclerosis. In a first aspect, the disclosure provides a method of treating or preventing amyotrophic lateral sclerosis associated with a mutation in the human superoxide dismutase 1 (SOD1) gene in a human subject in need thereof.SELECTED DRAWING: None
Resumen de: EP4570823A1
The present invention relates to an improved antibody specifically binding to amyloid-β oligomers (AβOs). Specifically, the present invention relates to an improved form of the antibody W20. Compared with the antibody W20, the improved form of the antibody W20 has a significantly improved affinity to AβOs, and can more significantly inhibit the aggregation of Aβ and the AβOs-induced toxicity of nerve cells, more effectively improve the cognition and memory functions of an Alzheimer's disease model mouse, and reduce pathological changes in the brain of the mouse. The improved form of the antibody can specifically bind to oligomers of an amyloid-β, α-synuclein, mHTT and SOD 1, can inhibit the aggregation and cytotoxicity of various amyloids, and has a better potential for treating various amyloid diseases, such as Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, than the antibody W20. The improved form of the antibody can specifically bind to a highly toxic amyloid protein oligomer Aβo*3F, and has a better AD diagnosis value. The amino acid sequence of the antibody W20 is as shown in SEQ ID NO: 1.
Resumen de: EP4570798A1
The present invention relates to an aromatic heterocycle-fused cyclohexyl aminoalkyl piperidine derivative, a preparation method and use thereof. Specifically, the present invention provides a compound of general formula (I), a stereoisomer thereof, a tautomer thereof, or a pharmaceutically acceptable salt thereof, and a preparation method therefor, use thereof for activating the activities of a 5-HT<sub>1A</sub> receptor and dopamine D<sub>2</sub> and D<sub>3</sub> receptors, and use thereof in the preparation of a medicament for Parkinson's disease.
Resumen de: EP4570793A1
The present invention relates to a new compound as a 5-HT<sub>2A</sub> receptor inverse agonist, a preparation method therefor and a pharmaceutical composition. The present invention further relates to the use of the compound or the pharmaceutical composition in the preparation of a drug for treating 5-HT<sub>2A</sub> receptor-related diseases. The diseases include non-motor symptoms caused by Parkinson's disease: delusions, hallucination, depression, anxiety, cognitive impairment and sleep disorders; dementia-related mental diseases; severe depression; or negative symptoms of schizophrenia, etc.
Resumen de: WO2025122565A1
Methods and compositions for treating neurodegenerative disorders comprising crRNA molecules targeting exon1a and/or intron 1 of C9ORF72 and a Cas13 protein or a polynucleotide encoding a Cas13 are provided.
Resumen de: WO2025122121A2
The present invention relates to a method (100) of synthesizing novel multi¬ effective urea/thiourea compounds which provide simultaneous inhibition of cholinesterase (AChE) and monoamine oxidase (MAO) enzymes known to play roles in Alzheimer's disease (AD); can interact with Ap peptides and/or P amyloid plaque; provide neuroprotective effect by reducing oxidative damage; and to the synthesized compounds and the biological activities they exhibit.
Resumen de: AU2023402123A1
The compositions of the present invention contain a novel aldehyde dehydrogenase derived from a novel mutant yeast, that improve memory and cognitive function. The present invention relates to a food and pharmaceutical composition for preventing Alzheimer's disease and Huntington disease by reducing the accumulation of lesional proteins in brain tissue. The food or pharmaceutical compositions of the present invention contain a lysate of any one or a mixture thereof selected from the group consisting of Saccharomyces cerevisiae, KCTC13925BP, KCTC14122BP, KCTC14123BP, KCTC14983BP, KCTC14984BP and KCTC14985BP.
Resumen de: WO2025120587A1
A composition for preventing and treating neurodegenerative diseases and cognitive disorders is provided, comprising a mixture of active ingredients, including choline bitartrate, Cordyceps, Hericium, and Bacopa.
Resumen de: US2025188158A1
A method of treating, preventing or ameliorating Parkinson's disease or the symptoms thereof, including motor and cognitive function-related symptoms, through the administration of an anti-synuclein antibody (e.g., Prasinezumab). Methods include maintaining motor function or cognitive function, and slowing decline in motor function and cognitive in a subject having Parkinson's disease or at risk of Parkinson's disease.
Resumen de: US2025186382A1
The present disclosure relates to compositions of levodopa 4′-monophosphate and carbidopa 4′-monophosphate having a weight by weight ratio of about 20:1 and methods of treating Parkinson's disease and associated conditions by subcutaneous administration of such compositions.
Resumen de: US2025186567A1
The disclosure provides peptide compositions and immunotherapy compositions comprising an amyloid-beta (Aβ, Abeta) peptide, a tau peptide, and an alpha-synuclein peptide. The disclosure also provides methods of treating or effecting prophylaxis of Alzheimer's disease or other diseases with beta-amyloid deposition in a subject, including methods of clearing deposits, inhibiting or reducing aggregation of Aβ and tau and an alpha-synuclein, blocking the uptake by neurons, clearing amyloid, and inhibiting propagation of tau seeds and an alpha-synuclein synucleinopathies in a subject having or at risk of developing Alzheimer's disease or other diseases containing tau and amyloid-beta and an alpha-synuclein accumulations. The methods include administering to such patients the compositions comprising an amyloid-beta (Aβ) peptide and a tau peptide and an alpha-synuclein peptide.
Resumen de: WO2025122530A1
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, for the treatment of subjects who have, have been diagnosed with having, 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: US2025186439A1
Provided herein are novel therapeutic applications of Pyk2 (PTK2B) inhibitors to treat low bone mineral density and/or osteoporosis and to treat, prevent, or delay the progression of neurodegenerative disorders such as Alzheimer's disease.
Resumen de: US2025186363A1
Pharmaceutical compositions and methods for treating and/or preventing and/or control of Parkinson's Disease and/or related symptoms in a patient.
Resumen de: AU2023403257A1
Provided herein are methods for treating Alzheimer' s disease using a combination of tramiprosate, a tramiprosate prodrug or an active tramiprosate metabolite with at least one amyloid plaque clearing agent.
Resumen de: WO2025122626A1
Hydrogen-bonded framework nanoparticles comprising a chemiluminescent compound (e.g., L-012) are provided and can be used, e.g., for sono-optogenetic treatment of neurodegenerative diseases such as Parkinson's disease. Related in vivo and therapeutic methods are also provided.
Resumen de: EP4566629A2
The present invention refers to a composition comprising human albumin at a concentration between 5 % (w/v) and 25 % (w/v) for the treatment of mild and moderate Alzheimer's Disease (AD) by low-volume plasma exchange (LVPE).
Resumen de: AU2023319981A1
The invention provides methods of treating patients with Parkinson's disease (PD) associated with wild-type LRRK2. The invention recognizes that analysis of biomarkers in such patients allows identification of those patients who will respond to LRRK2 inhibitors. Thus, the invention provides methods of identifying PD patients who will respond to LRRK2 inhibitors and methods of treating such patients.
Resumen de: WO2024153712A1
The present invention relates to a liposomal composition for use in a method of treating Parkinson's disease. The liposomal composition comprises sphingomyelin in a lipid bilayer and a therapeutically ef fective amount of monosialotetrahexosylganglioside (GM1), wherein a therapeutically ef fective dose of said liposomal composition is administered at most every 4 days in a primary mode of administration with at least 3 days between each administration; preferably at most every 6 days in a primary mode of administration with at least 5 days between each administration; most preferably at most every 7 days in a primary mode of administration with at least 6 days between each administration.
Nº publicación: US2025177568A1 05/06/2025
Solicitante:
KIRIK DENIZ [SE]
THE BOARD OF TRUSTEES OF THE LELAND STANFORD JUNIOR UNIV [US]
Kirik Deniz,
The Board of Trustees of the Leland Stanford Junior University
Resumen de: US2025177568A1
This disclosure provides recombinant DNA mol-encoding fusion proteins that are able to regulate expression of alpha-synuclein. Also provided are various compositions comprising the recombinant DNA molecules, as well as associated methods of use. The recombinant DNA molecules and associated methods are useful for the treatment of subjects having disorders caused by excess expression or intracellular accumulation of alpha-synuclein, including Parkinson's disease.
BOPI
Sede Electrónica
