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136
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Updated on
06/05/2025 [07:37:00]
Results 75 to 100 of 136
Absstract of: WO2025064229A1
The disclosure pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, the disclosure describes methods of assaying a sample obtained from a subject having or suspected of having a cognitive impairment for one or more proteins selected from: DLL1, VNN2, VAV3, and SUMF1. In certain embodiments, the cognitive impairment is caused by a neurodegenerative disease, such as Alzheimer's disease. The methods further comprise identifying a subject as likely or not likely to respond positively to the plasma exchange therapy. In even further aspects, the disclosure describes methods for treating a cognitive impairment in the subject by a plasma exchange therapy, wherein based on the specific protein expression data, the subject is identified as likely or not likely to respond positively to the plasma exchange therapy. The plasma exchange therapy can be full and/or low volume plasma exchange. Also provided are kits suitable for performing the methods disclosed herein.
Absstract of: WO2025063698A1
The present disclosure provides a pharmaceutical composition for the prevention, alleviation, or treatment of neurodegenerative disorders. The composition comprises a therapeutically effective amount of Lamotrigine and Rivastigmine, wherein the molar ratio of Rivastigmine to Lamotrigine is in the range from 1:1 to 1:50. The composition may be formulated for oral administration and can be used to treat neurodegenerative disorders such as Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and Alzheimer's disease. The disclosure also provides a method of treating neurodegenerative disorders using the composition and a kit containing separate formulations of Lamotrigine and Rivastigmine along with instructions for administration.
Absstract of: WO2025063407A1
The present application relates to a novel therapeutic agent for Parkinson's disease and a method for treating Parkinson's disease by using same.
Absstract of: US2025099434A1
Novel indane acetic acid compounds alone or in combination with anti-amyloid beta antibodies, for the treatment of Alzheimer's disease, for the reduction of Amyloid-related imaging abnormalities (ARIA), and for the treatment of Cerebral Amyloid Angiopathy and vasogenic edema (VE).
Absstract of: US2025101133A1
The present invention relates to isolated single domain antibodies having specificity for deNEDDylating enzyme NEDP1. It concerns in particular to a kit for inhibiting the deNEDDylating enzyme NEDP1, more particularly for the prevention and/or treatment of neurodegenerative diseases such as Amyotrophic Lateral Sclerosis and/or Frontotemporal Degeneration, said kit comprising at least one isolated single domain antibody specific for the deNEDDylating enzyme NEDP1. It further relates to said isolated single domain antibodies for use as inhibitors of the deNEDDylating enzyme NEDP1, in particular for the prevention and/or treatment of neurodegenerative diseases such as ALS/FTD.
Absstract of: US2025101026A1
Provided herein are compounds having a structure of Formula I, Formula II, or Table 1 as disclosed herein and methods of using the disclosed compounds to inhibit a beta amyloid (Aβ)-amyloid-binding alcohol dehydrogenase (ABAD) protein-protein interaction, such as to inhibit beta amyloid (Aβ)-amyloid-binding alcohol dehydrogenase (ABAD) binding. For example, the compounds of Formula I, Formula II, and Table 1 as disclosed herein are useful for methods of treating diseases and disorders including, without limitation, Alzheimer's disease, Parkinson's disease, motor neuron disease, or spinal muscular atrophy.
Absstract of: US2025101087A1
The present inventive concept is related to antibodies, such as recombinant humanized and monoclonal antibodies, methods of making antibodies, and methods of using antibodies, such as antibodies directed toward and capable of specifically binding to and clearing amyloid-beta (Aβ) plaques in the brain that are suitable for use in the treatment of disorders such as Alzheimer's Disease (AD).
Absstract of: US2025098723A1
A method of treating Alzheimer's associated pathology includes a step of identifying subject having a pathology that is associated with Alzheimer's disease. A fasting mimicking diet (FMD) is then administered to the subject for a first time period. Methods for treating amyloid plaque formation and/or elevated levels of tau protein as well as neuroinflammation are also provided.
Absstract of: US2025101018A1
Described herein are compounds of formula (I), and pharmaceutically acceptable salts, solvates, hydrates, isotopically labeled derivatives and radiolabeled derivative thereof, and pharmaceutical compositions thereof. Also provided are methods and kits involving the inventive compounds or compositions for detecting and imaging Tau aggregates in the brain for detection of Alzheimer's disease (AD) in a subject.
Absstract of: US2025099624A1
The present disclosure is in the field of modulation of genes involved in rare diseases including for diagnostics and therapeutics for rare diseases such as Angelman's Syndrome, Facioscapulohumeral Muscular Dystrophy (FHMD), Amyotrophic Lateral Sclerosis (ALS), Frontotemporal dementia (FTD) and Spinal Muscular Atrophy (SMA).
Absstract of: US2025099548A1
The present invention relates to a pharmaceutical composition for preventing or treating degenerative brain diseases by using glucagon-like peptide-1 (GLP-1) and an interleukin-1 receptor antagonist (IL-1Ra). A composition comprising a fusion protein including GLP-1 and IL-1Ra, according to the present invention, exhibits the effects of inhibiting the production of amyloid beta, which is known as a material causing Alzheimer's disease, and improving memory and cognitive function. In addition, it has been identified that when a bispecific antibody comprising GLP-1 and an anti-IL-1 antibody or a fusion protein in which IL-1Ra and Fc are linked is administered, amyloid beta plaque deposition in the brain is decreased and a neurogenesis promotion effect is exhibited in Alzheimer's disease model mice. Moreover, it has been identified that when GLP-1 and IL-1Ra are also co-administered, amyloid beta plaque deposition in the brain is decreased in Alzheimer's disease model mice. Therefore, the composition comprising GLP-1 and IL-1R, according to the present invention, can be effectively used in the prevention or treatment of degenerative brain diseases, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, and the alleviation of cognitive impairment.
Absstract of: US2025099550A1
A method for treating Alzheimer's disease and related dementias and for slowing or delaying aging and prolonging life, comprising reducing circulating IGF-1 levels by administering to the patient an effective amount of a human growth hormone receptor antagonist, comprising human growth hormone receptor antagonist G120K, wherein a single amino acid of the human growth hormone receptor antagonist G120K has been mutated to cysteine, and wherein the single amino acid mutated to cysteine is T142; and a polydispersed 40 kDa branched polyethylene glycol molecule conjugated to the substituted cysteine in the human growth hormone receptor antagonist G120K mutant, wherein reducing circulating IGF-1 levels reduces the effects of Alzheimer's disease and related dementias and slows or delays aging and prolongs life.
Absstract of: US2025099538A1
Disclosed herein are methods of preventing or treating ALS by use of a modified EKLF polypeptide, a modified nucleic acid encoding the modified EKLF polypeptide, or modified bone marrow cells comprising the modified nucleic acid. According to embodiments of the present disclosure, the modified EKLF polypeptide comprises an amino acid modification that confers reduced sumoylation in a wild-type EKLF polypeptide.
Absstract of: US2025101420A1
ProblemsTo provide a chemically modified siRNA that has improved stability against RNase enzymes and selectively exhibits silencing of FUS P525L mutation which is a causative gene of ALS.SolutionProvided is a chemically modified siRNA comprising a sense strand and an antisense strand, or a salt thereof, wherein: the antisense strand includes a complementary or substantially complementary region in a portion of a mRNA that codes FUS P525L mutation protein; the complementary region has a nucleotide length of 19 to 21; and the siRNA contains at least one substitution selected from the group consisting of a 2′-F-nucleotide, a 2′-OMe-nucleotide, a nucleotide in which a 2′-O atom and a 4′-O atom are bridged by methylene, a 2′-deoxynucleotide, and a phosphorothioate bond that forms an internucleotide bond.
Absstract of: AU2023342126A1
Described are 6-aryl isoindolin-1-ones as negative allosteric modulators of metabotropic glutamate receptor 2 (mGlu2), pharmaceutical compositions including the compounds, and methods of using the compounds and compositions for treating depression, anxiety, obsessivecompulsive disorder, cognitive disorders, Alzheimer's disease, or autism spectrum disorders in a subject.
Absstract of: AU2023338571A1
The compositions and methods described herein include methods and agents that inhibit inflammasome signaling in a mammal such as antibodies directed against inflammasome components used alone or in combination with extracellular vesicle uptake inhibitor(s) or other agents. Also described herein are compositions and methods of use thereof for detecting and treating early-stage Alzheimer's disease as well as other inflammatory neurologic conditions.
Absstract of: WO2025061205A1
Disclosed is a polypeptide for treating Parkinson's disease. It is found for the first time that the transient receptor potential melastatin 2 (TRPM2) channel is more highly expressed in fragile DA neuron subpopulations, and the expression level of the transient receptor potential melastatin 2 (TRPM2) channel is positively correlated with age in Parkinson's disease (PD) patients. Through rigorous experiments, the mechanism of action of the TRPM2 channel is clarified, that is, the TRPM2 channel is preferentially activated in the ADE neuron through the PARP-1/PARG/ADPR axis, which drives the Mfn2/Bcl-2 complex-dependent mitochondrial hyperfusion, thereby causing ADE neuron death. In addition, the TRPM2 channel also mediates, through the Mfn2/Bcl-2, the susceptibility of SNc DA neurons in MPTP-treated mice. It is found for the first time that blocking the DA neuron death pathway mediated by PARP-1/PARG/ADPR and Mfn2/Bcl-2 can prevent the death of induced pluripotent stem cell (iPSC)-derived DA neurons specific to spontaneous Parkinson's disease (SPD) patients. Since the loss of susceptible SNc DA neurons is a major symptom of PD, the PARP-1/PARG/ADPR and Mfn2/Bcl-2 pathway may become new therapeutic targets for PD.
Absstract of: WO2025065014A1
A method for treating Alzheimer's disease and related dementias and for slowing or delaying aging and prolonging life, comprising reducing circulating IGF-1 levels by administering to the patient an effective amount of a human growth hormone receptor antagonist, comprising human growth hormone receptor antagonist G120K, wherein a single amino acid of the human growth hormone receptor antagonist G120K has been mutated to cysteine, and wherein the single amino acid mutated to cysteine is T142; and a polydispersed 40 kDa branched polyethylene glycol molecule conjugated to the substituted cysteine in the human growth hormone receptor antagonist G120K mutant, wherein reducing circulating IGF-1 levels reduces the effects of Alzheimer's disease and related dementias and slows or delays aging and prolongs life.
Absstract of: CN119212693A
Provided herein are methods and compositions for the treatment of neurodegenerative diseases (e.g., ALS). The methods may comprise administering to the subject a bile acid or a pharmaceutically acceptable salt thereof and a phenylbutyric acid compound.
Absstract of: WO2023225244A1
The present disclosure provides a compound of Formula (I) or a pharmaceutically acceptable salt thereof and its use in, e.g. treating a condition, disease, or disorder in which lowering mutant huntingtin protein ("mHTT") in a subject is of therapeutic benefit, specifically in treating Huntington disease ("HD"). This disclosure also features a composition containing the same as well as methods of using and making the same.
Absstract of: WO2023222924A1
The present invention concerns Lachnospiraceae spp and Ruminococcus lactaris new strains of bacteria for use solely or in combination, in the treatment and prevention of memory decline in an individual, in particular declines of aging or Alzheimer's disease-related origin. The present invention also provides compositions, in particular, an oral composition, comprising the Lachnospiraceae spp and Ruminococcus lactaris strains and uses thereof.
Absstract of: EP4528274A2
The invention relates to the use of biomarkers of TrkB-FL, TrkB-ICD, TrkB-T', the TrkB-T':TrkB-FL ratio, or the TrkB-ICD:TrkB-FL ratio in the in vitro diagnosis of Alzheimer Disease (AD) or for determining the stage of AD, methods for their use, methods of diagnosis, methods of monitoring disease progression, in neuropathological diseases, in particular for Alzheimer's disease.
Absstract of: WO2025059104A1
Described are methods of treating a neurodegenerative disease, such as an age- related neurodegenerative disease in a patient in need thereof, comprising administering a composition comprising a therapeutically effective amount of at least one human milk oligosaccharide (HMO). Also described are methods of treating Parkinson's Disease (PD) in a patient in need thereof comprising administering to said patient an effective amount of an HMO.
Absstract of: AU2025201530A1
The present disclosure is in the field of modulation of genes involved in rare diseases including for diagnostics and therapeutics for rare diseases such as Angelman's Syndrome, 5 Facioscapulohumeral Muscular Dystrophy (FHMD), Amyotrophic Lateral Sclerosis (ALS), Frontotemporal dementia (FTD) and Spinal Muscular Atrophy (SMA).
Nº publicación: WO2025059486A1 20/03/2025
Applicant:
PROTHENA BIOSCIENCES LTD [IE]
NIJJAR TARLOCHAN S [US]
TAM STEPHEN JED [US]
PROTHENA BIOSCIENCES LIMITED,
NIJJAR, Tarlochan S,
TAM, Stephen Jed
Absstract of: WO2025059486A1
The present disclosure provides antibodies that specifically bind to human TDP-43 and methods of using these antibodies to treat patients with TDP-43-related diseases, including Amyotrophic Lateral Sclerosis (ALS).
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