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122
resultados
Última actualización
16/06/2025 [07:45:00]
Resultados 75 a 100 de 122
Resumen de: WO2025097123A1
Aspects of the invention are drawn to methods for identifying or treating Alzheimer's Disease and/or Alzheimer's Disease and Related Dementias (AD/ADRD) in a subject. Further aspects of the invention are drawn to methods for screening the presence of an Alzheimer's Disease and/or Alzheimer's Disease and Related Dementias (AD/ADRD) signature.
Resumen de: WO2025097160A1
The present disclosure provides methods of enhancing levodopa therapeutic efficacy for the treatment of Parkinson's disease. The present methods can include administration of compounds having a triphenylphosphonium moiety. Advantageously, the present method can mitigate microbial metabolism of levodopa to dopamine in the gut, improve bioavailability of levodopa in brain, and increase dopamine levels in the brain.
Resumen de: WO2025095553A1
A pharmaceutical composition for preventing or treating dementia diseases, containing, as an active ingredient, an isoquinoline derivative compound or a pharmaceutically acceptable salt thereof, of the present invention, does not induce cytotoxicity and can alleviate learning and memory abnormalities in an animal model of Alzheimer's dementia, and thus is expected to be effectively used in the development of therapeutic agents for dementia diseases.
Resumen de: EP4549579A1
A composition of the present disclosure contains edaravone and is used for causing a change in expression level of a gene product in a target. The gene product is a gene product of one or more genes selected from KAZALD1, SBK1, SCN2A, UBE2L6, ALPL, NTM, PTTG1, ITGB4, HAUS4, DCTD, MT2A, ASF1B, FCSK, MAST1 and FAIM2. The composition is also suitably used as a pharmaceutical. The composition is also suitably used for treating or preventing a neurodegenerative disease. The neurodegenerative disease is suitably amyotrophic lateral sclerosis (ALS). The present disclosure also provides a method for evaluating responsiveness of edaravone based on an expression level of the gene product or a change in the expression level.
Resumen de: EP4549585A1
A kit for diagnosing Alzheimer's disease and a pharmaceutical composition for treating Alzheimer's disease are disclosed, in which EDIL3 or a nucleic acid encoding EDIL3 is used as an index or target.
Resumen de: NZ776663A
A method of determining the epigenetic chromosome interactions which are relevant to a companion diagnostic. In particular, the present invention relates to an in vitro method for determining predisposition to amyotrophic lateral sclerosis in a person, wherein the method comprises detecting the presence or absence of epigenetic chromosome interaction markers.
Resumen de: NZ746628A
The present invention provides a compound having an MAGL inhibitory action, and useful as an agent for the prophylaxis or treatment of neurodegenerative diseases (e.g., Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, traumatic brain injury, glaucoma, multiple sclerosis etc.), anxiety disorder, pains (e.g., inflammatory pain, cancerous pain, neurogenic pain etc.), epilepsy, depression and the like. The present invention relates to a compound represented by the formula (I) : wherein each symbol is as defined in the specification, or a salt thereof.
Resumen de: WO2025090815A1
The application describes a phosphorylated tau targeted active Immunotherapy to treat preclinical Alzheimer's Disease.
Resumen de: AU2023406056A1
Disclosed herein are methods of diagnosing, selecting, monitoring, and treating subjects with Alzheimer's disease (AD) or suspected of having AD or another disorder associated with amyloid accumulation in the brain using a tau PET level.
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: 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: 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: 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: AU2023347329A1
This disclosure relates to, inter alia, certain compounds, compositions, and pharmaceutical compositions thereof, that modulate the activity of the transporter protein vesicular monoamine transporter-2 (VMAT2) and are directed to methods useful in the treatment of transporter protein vesicular monoamine transporter-2 mediated disorders, such as, neurological or psychiatric disease or disorders, including but not limited to, hyperkinetic movement disorders (e.g., tardive dyskinesia, Tourette's syndrome, Huntington's disease, tics, ataxia, chorea (such as, chorea associated with Huntington's disease), dystonia, hemifacial spasm, myoclonus, restless leg syndrome, and tremors). The disclosure further relates to synthetic methods and intermediates useful in the preparation of the compounds.
Resumen de: WO2025087971A1
The invention relates to the treatment of Alzheimer's disease in a human patient, said treatment comprising administration of an anti-Aβ antibody component and co-administration of edaravone, the anti-Aβ antibody component being selected from anti-Aβ antibody, an Aβ- binding fragment of an Aβ antibody, a vectorised anti-Aβ antibody and a vectorised Aβ- binding fragment of an Aβ antibody.
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: KR20250056106A
본 발명은 Lin28A 억제제를 유효성분으로 포함하는 헌팅턴병 지연 또는 치료용 조성물에 대한 것으로, 본 발명은 헌팅턴병 특이적으로 많이 분비되는 Lin28A의 발현을 억제함으로써, 헌팅턴병 예방 또는 치료 효과를 가질 수 있는 다양한 억제제 및 이의 스크리닝 방법에 대한 것이다.
Resumen de: US2025129158A1
The invention provides compositions and methods for suppressing autoimmune components of neurodegenerative diseases and thereby providing therapeutic effects to patients suffering from such diseases. Compositions and methods include immunosuppressive moieties such as regulatory T cells (Tregs) and proteins expressed by Tregs coupled to a chimeric antigen receptor or protein that specifically binds one or more glial cell markers. Therapeutically effective doses of said compounds for treating neurodegenerative diseases including progressive supranuclear palsy (PSP), Parkinson's disease (PD), Alzheimer's, Huntington's disease, amyotrophic lateral sclerosis (ALS), chronic traumatic encephalopathy (CTE), and prion diseases are disclosed.
Resumen de: WO2025083211A1
The inventors hypothesized that inhibition of complement activation could reduce the inflammatory period observed even before clinical signs of Alzheimer's disease and thus slow down the onset and progression of AD. In order to validate the hypothesis, the inventors injected Factor H (FH: the main inhibitor of complement activation) into the brain of APP/PS1 AD- mice model at early or late stage of this pathology. The results showed effects of FH brain injection on the AD-onset as well as progression by reducing pro-inflammatory IL6, TNF-α, Il1β, MAC and Aβ levels associated with an increase of VGLUT1 and Psd95 neurotransmitters levels in hippocampal region leading to improvement of cognitive functions even at late stage of the pathology. The results thus prompt the inventors to consider that FH would be suitable for the treatment of dementia, and more particularly for the curative treatment of dementia.
Nº publicación: US2025127775A1 24/04/2025
Solicitante:
PETCAVICH ROBERT JOHN [US]
Petcavich Robert John
Resumen de: US2025127775A1
The present invention discloses a method to recover and restore dendritic and synaptic neuron connections that have been degraded or destroyed by neurodegenerative diseases. In the present invention tryptamines are used to induce neuro plasticity and restore both dendritic density and synaptic connections of neurons in the brain. In the preferred embodiment LSD given in micro doses can induce dendritic and synaptic genesis in neuronal networks and improve the quality of life of people with neurodegenerative diseases such as Alzheimer's, Huntington's, Multiple Sclerosis, Parkinson's and Frontotemporal dementia.
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