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123
results.
Updated on
07/06/2025 [06:51:00]
Results 50 to 75 of 123
Absstract of: WO2025093735A2
The present invention relates to an agent for use in decreasing the level of intracellular phosphorylated tau in neurons, which agent can bind ELAVL4 with a binding affinity of at least - 8.0 kcal/mol. The agent comprises a structural element selected from the group consisting of a steroid backbone, a sugar moiety by glycosidic linkage, an O-linked glucuronide, and a lactone group and is suitably selected from the group of porphyrins, macrolactams, macrolides, vitamin D glucuronides, steroid glucuronides, withanolides, cardenolide glycosides, anthracyclines, ergoloid mesylates, ergotamines and derivates thereof, biphenyls, and piperazines. The administration of said agent leads to a decrease in protein levels of phosphorylated tau in normal neurons treated with the agent as compared to non-treated normal neurons and to a decrease in the Aβ42/Aβ40 ratio in fAD neurons treated with the agent as compared to non-treated fAD neurons. The agent is administered for the treatment of a tauopathy, which may be involved in Alzheimer's disease, frontotemporal dementia, Parkinson's disease or progressive supranuclear palsy and multiple sclerosis.
Absstract of: KR20250063452A
본 발명은 상염색체우성 알츠하이머병에서 노화 조절을 통한 아밀로이드 병리 제거에 최적 시기 및 방법을 확인하여 완성된 것으로서, 노화세포 표적 약물을 진행된 알츠하이머병 환자에 투여하여 알츠하이머병을 치료하는 방법 등을 제공하여 노화 조절을 통한 새로운 패러다임의 알츠하이머병의 치료적 접근을 가능하게 하며, 상기 방법의 효과적인 치료시기를 제공함으로써 진행된 알츠하이머병 환자를 대상으로 하는 다각적 치료방법의 하나로 이용될 수 있다.
Absstract of: US2025146000A1
The present invention relates to small interfering RNA (siRNA) molecules against the SOD1 gene, adeno-associated viral (AAV) vectors encoding siRNA molecules and methods for treating amyotrophic lateral sclerosis (ALS) using the siRNA molecules and AAV vectors.
Absstract of: 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.
Absstract of: US2025144159A1
A composition comprising a mixture of DHA and/or EPA in the form of glyceride or ethylester derived from at least one microorganism, such as a microalga, and at least one plant-derived phospholipid, in which the content of DHA and/or EPA in triglyceride form is between 10% and 90% by weight relative to the total weight of the composition, and the content of at least one plant-derived phospholipid, such as phosphatidylcholine, is between 10% and 90% by weight relative to the weight of composition. The method for manufacturing same and to the use thereof, in particular in the treatment of pathologies involving a deficiency of DHA and/or EPA, such as age-related macular degeneration or Alzheimer's disease.
Absstract of: US2025144135A1
The present invention provides a method of treating frontotemporal dementia, or a childhood genetic neurodegenerative disease such as Ataxia Telangiectasia (A-T), or neurodegenerative diseases such as Parkinson's disease or neuropsychiatric diseases comprising administering to a subject in need thereof an effective amount of chlorite composition, such as sodium chlorite. The present invention thereby provides a method of modulating the immune system in a subject in need thereof. Described herein are methods of administration and treatment.
Absstract of: US2025145695A1
The present invention is in the field of transactive response DNA binding protein with a molecular weight of 43 kDa (TARDB or also TDP-43). The invention relates to humanized TDP-43 specific binding molecules, in particular to humanized anti-TDP-43 antibodies or antigen-binding fragment or a derivative thereof and uses thereof. The present invention provides means and methods to diagnose, prevent, alleviate and/or treat a disease, disorder and/or abnormality associated with TDP-43 aggregates including but not limited to Frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), Parkinson's disease (PD), Chronic Traumatic Encephalopathy (CTE), and limbic-predominant age-related TDP-43 encephalopathy (LATE).
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: US2025135034A1
Compositions and methods are provided for the treatment or prophylaxis of amyloid pathologies such as Alzheimer's Disease.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Absstract of: 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.
Nº publicación: WO2025090815A1 01/05/2025
Applicant:
JANSSEN PHARMACEUTICALS INC [US]
AC IMMUNE SA [CH]
JANSSEN PHARMACEUTICALS, INC,
AC IMMUNE SA
Absstract of: WO2025090815A1
The application describes a phosphorylated tau targeted active Immunotherapy to treat preclinical Alzheimer's Disease.
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