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145
resultados
Última actualización
28/06/2025 [08:48:00]
Resultados 125 a 145 de 145
Resumen de: US2025134863A1
Disclosed is a medical agent for treating or suppressing progression of at least one symptom selected from a group consisting of amyotrophic lateral sclerosis and symptoms resulting from amyotrophic lateral sclerosis in a subject. The medical agent contains 3-methyl-1-phenyl-2-pyrazolin-5-one or a physiologically acceptable salt thereof, or a hydrate or solvate thereof. A blood uric acid level of the subject before administration of the medical agent is 4.2 mg/dL or higher.
Resumen de: US2025135034A1
Compositions and methods are provided for the treatment or prophylaxis of amyloid pathologies such as Alzheimer's Disease.
Resumen de: US2025136993A1
The present invention relates to antisense oligonucleotides that are complimentary to SOD1, leading to decreased expression of SOD1. Reduced expression of SOD1 is beneficial in medical disorders such as Amyotrophic Lateral Sclerosis.
Resumen de: US2025134894A1
The present invention provides a composition for preventing or treating a neurodegenerative disease containing a phosphodiesterase 5 inhibitor (PDE5 inhibitor) and an N-methyl-D-aspartate-receptor (NMDA-receptor) antagonist and a method using thereof, wherein the PDE5 inhibitor is mirodenafil, sildenafil, vardenafil, tadalafil, udenafil, dasantafil, avanafil, pharmaceutically acceptable salts, solvates, hydrates, or a mixture thereof; and the NMDA-receptor antagonist is selected from among memantine, amantadine, ketamine, traxoprodil, lanicemine, rislenemdaz, pethidine, levorphanol, methadone, dextropropoxyphene, tramadol, ketobemidone, dextromethorphan (DXM), phencyclidine (PCP), and methoxetamine (MXE), pharmaceutically acceptable salts, solvates, hydrates and a mixture thereof; and the neurodegenerative disease is dementia, Parkinson's disease (PD), Dementia with Lewy body (DLB), Alzheimer's disease (AD), Huntington's disease (HD), Multiple sclerosis (MS), Vascular Dementia (VaD), Amyotrophic Lateral Sclerosis (ALS), frontotemporal dementia, or a mixed etiologies thereof.
Resumen de: WO2025085971A1
The present disclosure provides human Tau protein (Tau)-binding proteins comprising an antigen binding domain of an antibody, wherein the antigen binding domain binds specifically to an epitope of Tau that results in inhibition of Tau aggregate seeding, and could be used to inhibit spreading of Tau aggregates in vivo. Also disclosed herein are nucleic acids, expression vectors, and recombinant viruses encoding such Tau-binding proteins, as well as compositions comprising such Tau-binding proteins. Also disclosed are methods for use of such compositions in the diagnosis, prophylaxis, treatment, and prognosis of Tauopathies such as Alzheimer's Disease, frontotemporal dementia, Pick's disease, and progressive supranuclear palsy. Genetically modified cells for expression for the disclosed Tau-binding proteins, and their use for production of the Tau-binding proteins are also disclosed.
Resumen de: WO2025090815A1
The application describes a phosphorylated tau targeted active Immunotherapy to treat preclinical Alzheimer's Disease.
Resumen de: WO2025090567A1
A composition for treating Huntington's disease (HD) by reducing endogenous Huntingtin (HTT) levels in a target includes a siRNA including a siRNA sequence selected from SEQ ID NOs:47 to 149, and a carrier peptide comprising a peptide sequence of SEQ ID NO:1. The carrier peptide may target the nicotinic acetylcholine receptor (nAChR) of neuronal cells in order to deliver the siRNA across the blood-brain barrier (BBB). In some embodiments, the siRNA may be conjugated with the carrier peptide. A method of reducing endogenous HTT levels to treat HD in the target may include administering a composition including a siRNA sequence selected from SEQ ID NOs: 47 to 149 to the target.
Resumen de: WO2025090442A1
Methods and compositions for promoting neuroprotection and/or reducing neuronal death are provided. In some aspects, gene therapies to overexpress yin-yang 1 (YY1) are provided and can be used to decrease death of dopaminergic neurons during a neurodegenerative disease, such as Parkinson's disease, or after trauma.
Resumen de: WO2025088613A1
Provided are methods of treating a subject having a disease characterized by accumulation of FUS -associated aggregates by administering to the subject a therapeutically effective amount of a proteasome inhibitor, an agent which upregulates SAT1, or an agent which upregulates spermine, thereby treating the subject. Also provided are proteasome inhibitors, an agent which upregulates SAT1, or an agent which upregulates spermine for use in treating a subject having a disease characterized by accumulation of FUS-associated aggregates, and methods of reducing accumulation of FUS-associated aggregates in cells of a subject, the method comprising contacting the cells of the subject with a proteasome inhibitor an agent which upregulates SAT1, or an agent which upregulates spermine, thereby reducing the accumulation of FUS-associated aggregates in the cells of the subject.
Resumen de: EP4545071A1
A sustained-release microsphere containing a drug, pamoic acid, and a biocompatible polymer, a pharmaceutical composition containing the sustained-release microsphere for prevention, improvement, or treatment of hepatitis B, prostate cancer, breast cancer, endometriosis, uterine fibroid, precocious puberty, acromegaly, gastro·entero·pancreatic endocrine tumor, Alzheimer's disease, or cognitive disorder, and a preparing method of the sustained-release microsphere are provided.
Resumen de: WO2023250249A1
As described herein, inhibitors of High mobility group box protein 1 (HMGB1) can significantly reduce HMGB1 nucleo-cytoplasmic translocation, gliosis, neurodegeneration, Tau pathologies, and myelin deficits, especially in subjects having an AP0E4 allele. Methods are therefore described herein that include administering one or more inhibitors of High mobility group box protein 1 (HMGB1) to a subject having at least one genomic AP0E4 allele.
Resumen de: CN119907661A
The present invention relates to a pharmaceutical composition containing sustained release microspheres composed of semeglutide or a pharmacologically acceptable salt thereof, a bioavailability enhancer and a biodegradable polymer, which is designed to avoid rapid initial drug release (initial burst release), contains a high concentration of drug with respect to particle size, has high bioavailability, and can be used in the field of pharmaceutical preparations. And when the composition is applied to a human body, discomfort and inflammatory response of a patient are reduced as much as possible, so that the composition can be used for preventing or treating degenerative nervous system diseases such as diabetes, hypertension, hyperlipidemia, obesity, non-alcoholic steatohepatitis or Alzheimer's disease and Parkinson's disease and can be used for protecting beta cell functions.
Resumen de: CN119896720A
The invention discloses application of royal jelly protein in a medicine for treating Alzheimer's disease. The application comprises the following steps: S1, extracting royal jelly protein; s2, preparing medicine raw materials; s3, mixing the raw materials: mixing the raw materials to obtain a mixed raw material medicine; and S4, adding water into the mixed raw material medicine, decocting twice, filtering after each time of decoction, combining the two filtrates, and concentrating under reduced pressure to obtain an extract, namely the royal jelly protein-containing medicine for treating the Alzheimer's disease. The invention further discloses preparation equipment of the royal jelly protein in the medicine for treating the Alzheimer's disease. The royal jelly protein is applied to the medicine for treating the Alzheimer's disease, and the royal jelly protein is rich in vitamin B and a large amount of protein, has a very strong bactericidal ability, has an effect of inhibiting the growth of cancer cells, can improve nutrition, supplement brain power and promote metabolism of a human body, and can be used for treating the Alzheimer's disease. Therefore, the effect of treating the Alzheimer's disease can be improved, and the occurrence probability of the Alzheimer's disease is reduced.
Resumen de: CN119899264A
The invention provides a monoclonal antibody of a p-Tau181 protein and an application of the monoclonal antibody. Specifically, the invention provides an antibody targeting p-Tau181 protein or an antigen binding fragment of the antibody. The antibody provided by the invention can specifically recognize and bind the p-Tau181 protein, does not recognize p-Tau217 and non-phosphorylated Tau protein, and can be used for preparing a detection preparation or a kit for diagnosing diseases related to the p-Tau181 protein, such as Alzheimer's disease.
Resumen de: CN119907664A
A method of treating Parkinson's disease in a patient that accepts N doses per day of levodopa to provide X mg total daily dose of levodopa and that begins to experience motion fluctuations or begin to show a sign of "hypoefficacy", the treatment comprises administering more than N doses per day of levodopa to provide X mg of a total daily dose of levodopa, and administering Y mg of opirapone in a single daily dose, where X is from 100 to 1000, N is from 2 to 10, and Y is from 25 to 50.
Resumen de: CN119896751A
The invention features the use of an adenylate deaminase base editor to destroy the scissor acceptor site of a disease-related gene, including compositions and methods for treating genetic diseases, particularly for treating, alleviating or ameliorating the asthenic effect of amyotrophic lateral sclerosis (ALS) and spinal bulbar muscular atrophy (SBMA). Provided herein are compositions and methods for using improved new base editors (e.g., adenosine base editors) comprising a polynucleotide programmable nucleotide binding domain and a nucleobase editing domain that cooperate with a guide polynucleotide, e.g., adenosine base editors, for example, adenosine base editors, for example, adenosine base editors, for example, adenosine base editors, for example, adenosine base editors, for example, adenosine base editors. The present invention relates to a method for modifying a target gene associated with a hereditary disease or disorder, such as ALS or SBMA, by modifying the target gene using a base editor system provided herein to disrupt normal transcription of a gene associated with the hereditary disease or disorder.
Resumen de: CN119896737A
The invention discloses a novel exosome composition as well as a preparation method and application thereof, and belongs to the technical field of biological medicines. The composition is obtained by mixing exosome, nicotinamide adenine dinucleotide or a precursor thereof and ginsenoside, can play a synergistic effect of different action mechanisms, and can significantly enhance the cognitive function to treat diseases related to brain hypofunction compared with single use of one component. Moreover, the components are all natural products existing in the nature, and clinical intravenous injection products have better safety in actual use. The composition can be applied to preparation of products for treating brain memory hypofunction, and is used for treating brain hypofunction caused by memory hypofunction, Alzheimer's disease, ischemic cerebral apoplexy sequelae and the like. The invention provides a detailed product preparation method and use guidance, and the effectiveness and safety of the traditional Chinese medicine composition are verified through a product pharmacodynamic embodiment.
Resumen de: CN119907800A
The present disclosure relates, inter alia, to certain compounds, compositions, and pharmaceutical compositions thereof that modulate the activity of transporter vesicular monoamine transporter 2 (VMAT2), and to methods for treating transporter vesicular monoamine transporter 2 mediated disorders, such as neurological or psychiatric diseases or disorders, including but not limited to hyperdyskinesia (e.g., hyperdyskinesia). Delayed dyskinesia, Tourette's Syndrome, Huntington's Disease, twitch, ataxia, chorea (such as chorea associated with Huntington's Disease), muscular dystonia, lateral spasm, muscular spasm, restless leg Syndrome, and tremor). The present disclosure also relates to synthetic processes and intermediates useful for preparing the compounds.
Resumen de: CN119907802A
The present application relates to pyrrolo-triazine and imidazo-triazine derivatives of general formula (I) for use in the treatment, amelioration or prevention of a group of diseases, disorders and abnormalities responsive to modulation of components of the NLRP3 inflammasome pathway or inhibition of activation thereof. Specifically, the component of the inflammasome pathway is an NOD-like receptor (NLR) family, a protein 3 (NLRP3) inflammasome containing a thermal protein domain. More specifically, the compounds have the ability to modulate the NLRP3 inflammasome pathway and are suitable for treating, ameliorating or preventing a group of diseases, disorders and abnormalities responsive to modulation, in particular reduction, of IL-1 beta and/or IL-18 levels, such as Alzheimer's disease, Parkinson's disease, non-alcoholic fatty liver disease and gout. # imgabs0 #
Nº publicación: CN119899184A 29/04/2025
Solicitante:
GENERAL HOSPITAL OF NORTHERN THEATER COMMAND OF PLA
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Resumen de: CN119899184A
The invention belongs to the technical field of organic compound synthesis and medical application, and particularly relates to a beta-carboline compound as well as a preparation method and application thereof in resisting Alzheimer's disease. The structural general formula of the compound is shown as a formula I or a formula II. The beta-carboline compound provided by the invention can selectively inhibit the enzyme activity of GSK-3beta and improve cognitive impairment of mouse Alzheimer's disease. Therefore, the compound plays an important role in preparation of drugs for preventing or treating Alzheimer's disease. # imgabs0 #
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