Resumen de: WO2025031917A1
The present disclosure provides certain piperidinylpyridinylcarbonitrile derivatives, and pharmaceutically acceptable salts thereof, that are inhibitors of Glutaminyl-peptide cyclotransferase (QPCT) and glutaminyl-peptide cyclotransferase-like protein (QPCTL), and are therefore useful for the treatment of diseases treatable by inhibition of QPCT/L. Also provided are pharmaceutical compositions containing the same, and processes for preparing said compounds.
Resumen de: EP4755391A1
0001 Neurological disorders, Parkinson's disease and Multiple System Atrophy (MSA) cause serious socio-economic problems as there are, at present only therapies that treat the symptoms. Parkinson's research is a highly competitive field focusing on the specific drug targeting of the aggregation of alpha-synuclein (SYN). The discovery of Tubulin Polymerization Promoting Protein (TPPP) was a crucial factor in anti-Parkinson research. TPPP is a prominent pathological partner of SYN, which shifts the SYN-SYN aggregation toward the formation of fatal SYN-TPPP assemblies. The disassembly of the SYN-TPPP by specific agents may eliminate the toxicity of the pathological assembly of SYN by the proteolytic degradation of the excess SYN and leads to the recovery of the physiologically active proteins.
Resumen de: US2025059165A1
0000 The present disclosure provides certain piperidinylpyridinylcarbonitrile derivatives, and pharmaceutically acceptable salts thereof, that are inhibitors of Glutaminyl-peptide cyclotransferase (QPCT) and glutaminyl-peptide cyclotransferase-like protein (QPCTL), and are therefore useful for the treatment of diseases treatable by inhibition of QPCT/L. Also provided are pharmaceutical compositions containing the same, and processes for preparing said compounds.
Resumen de: WO2026114612A1
The present invention relates to compounds of formula (I) as TMEM175 modulators for reducing alpha-synuclein aggregation for the treatment of Parkinson's disease.
Resumen de: US20260151515A1
Among the various aspects of the present disclosure is the provision of sigma-1 compounds, their radioligands, and related methods of use. The present teachings include compositions for compounds that target the sigma-1 receptor, as well as their radioligands. The present teachings also include a method to assess treatment efficacy of a sigma-1 modulator in a subject in need, which can include acquiring medical images after administration of a sigma-1 radioligand, characterizing sigma-1 expression from the acquired images, and assessing treatment efficacy of a sigma-1 modulator in the subject based on the assessed sigma-1 expression. The methods can assess treatment efficacy in neurological diseases, including but not limited to Alzheimer's disease.
Resumen de: WO2026114055A1
Provided are a hydroxymethyltransferase and a use of a cofactor or metabolic substrate thereof in preparation of drugs for treating neurodegenerative diseases. Specifically, a hydroxymethyl transfer reaction is performed on glycine residues in protein aggregates such as Poly-GA, Poly-GR, and TDP-43 by means of serine hydroxymethyltransferase 1 (SHMT1) and serine hydroxymethyltransferase 2 (SHMT2), so that the aggregates are degraded, thereby reducing pathological aggregation, and thus ameliorating the pathological condition of patients with neurodegenerative diseases such as ALS and FTD and delaying disease progression. A cofactor and a metabolic substrate of the hydroxymethyltransferase can promote the activity of the hydroxymethyltransferase, thereby enhancing the hydroxymethyl transfer effect on the aggregates such as Poly-GA, Poly-GR and TDP-43, and thus can also be used for treatment of the neurodegenerative diseases such as ALS and FTD.
Resumen de: AU2025321641A1
The present invention provides a use of lactoferrin in combination with ergothioneine in the preparation of a drug for preventing and/or treating Alzheimer's disease. Compared with the use of lactoferrin or ergothioneine alone, in the present invention, the combined use of lactoferrin and ergothioneine at a specific ratio as an active pharmaceutical ingredient can reduce cell damage caused by Aβ25-35, reduce the expression of a p-Tau protein, lower the oxidative stress level and regulate apoptosis, alleviate memory impairment and cognitive dysfunction, and can reduce Aβ deposition in mouse plasma.
Resumen de: US20260151441A1
The present invention relates to a composition for preventing, alleviating or treating cognitive impairment or Alzheimer's disease, comprising a Lactobacillus delbrueckii subsp. lactis strain as an active ingredient. The present invention provides a composition for preventing, alleviating or treating cognitive impairment or Alzheimer's disease (AD), comprising a Lactobacillus delbrueckii subsp. lactis strain as an active ingredient. The strain of the present invention has the excellent effects of reducing amyloid beta protein (Aβ) or tau protein (Tau) and improving cognitive function, and thus can be effectively used as a composition for preventing, alleviating or treating cognitive impairment or AD.
Resumen de: US20260151390A1
The present disclosure provides diazaspiro compounds represented by Formula (I), processes for their preparation, and pharmaceutical uses thereof, all within the field of medicinal chemistry. The diazaspiro compounds disclosed herein function as small-molecule agonists of the cholecystokinin-B receptor (CCK-BR). They exhibit excellent agonistic potency and demonstrate marked selectivity for CCK-BR over the cholecystokinin-A receptor (CCK-AR), thereby mitigating off-target effects and associated adverse reactions. No cardiotoxicity or other safety liabilities have been observed to date. The diazaspiro compounds are contemplated for the prophylaxis or treatment of disorders including, without limitation, epilepsy, depression, dementia, anxiety, Alzheimer's disease, tinnitus, amblyopia, schizophrenia, neuropathic pain, amnesia, gastric hyperacidity, obesity, pancreatic carcinoma, and gallbladder carcinoma.
Resumen de: WO2026112879A1
The present invention provides a pyranone compound represented by formula (I). The pyranone compound has excellent anti-inflammatory activity and cholinesterase inhibitory activity, features a high blood-brain barrier penetration potential and good safety, and can ameliorate cognitive impairment related to Alzheimer's disease, reduce glial cell activation, decrease Aβ deposition and alleviate neuroinflammation.
Resumen de: AU2024379687A1
The present invention relates to a heterocyclic carbonyl derivative modulator, a preparation method therefor, and the use thereof. Specifically, the present invention relates to a compound represented by general formula (II-B), a preparation method therefor, a pharmaceutical composition containing said compound, and a use thereof as a modulator in the treatment of Alzheimer's disease, schizophrenia, pain, addiction, and sleep disorders, wherein each substituent in general formula (II-B) is as defined in the description.
Resumen de: AU2024367865A1
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: US20260151348A1
0000 The invention relates to engineered umbilical cord mesenchymal stem cell exosomes (hUCMSC-EVs) loaded with siCCR5, their preparation method, and their use in treating Alzheimer's disease. A lipid membrane is first prepared and dissolved, followed by incorporation of siCCR5 and hUCMSC-EVs. Using a cationic liposome extrusion technique, siCCR5 is efficiently delivered into the exosomes to obtain siCCR5-loaded engineered EVs. The resulting exosomes promote tissue regeneration, repair brain tissue, and modulate the brain microenvironment without causing toxicity. By carrying siCCR5, which targets a specific gene, the engineered EVs exhibit stronger targeted therapeutic effects and enhanced anti-inflammatory activity compared to conventional hUCMSC-EVs, thereby improving Alzheimer's disease progression.
Resumen de: WO2026117675A1
Methods for treating and preventing Parkinson's disease have been developed wherein allopregnanolone is administered to a human in need thereof in an amount between about 2 mg and about 6 mg, preferably 4 mg per dose. The methods include administering a dosage of from 2 mg to 6 mg, preferably 4 mg, to the subject once within a 24 hour period. The dosing is repeated every seven days, or less frequently.
Resumen de: WO2026112697A1
The present disclosure relates to a method of treating or ameliorating symptoms of a motor neurone disease and improving motor neuron survival in a subject, more specifically treating or ameliorating symptoms of amyotrophic lateral sclerosis (ALS) and related neurodegenerative disorders. The treatment method comprises administering a Janus kinase (JAK) inhibitor in combination with one or more compounds selected from a glutamate antagonist and an N-methyl-D-aspartate (NMDA) receptor antagonist, in particular baricitinib in combination with riluzole and/or memantine, and compositions and kits thereof for same.
Resumen de: US20260152744A1
Disclosed herein are compositions and methods for reducing expression of C9ORF72 mRNA and protein in an animal with C9ORF72 specific inhibitors. Such methods are useful to treat, prevent, or ameliorate neurodegenerative diseases in an individual in need thereof. Such C9ORF72 specific inhibitors include antisense compounds. Examples of neurodegenerative diseases that can be treated, prevented, and ameliorated with the administration C9ORF72 specific inhibitors include amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), corticalbasal degeneration syndrome (CBD), atypical Parkinsonian syndrome, and olivopontocerellar degeneration (OPCD).
Resumen de: WO2026112688A1
Disclosed herein are methods for treating a motor neuron disease such as amyotrophic lateral sclerosis (ALS) comprising administering mEphA4-Fc with an interval of greater than every week, for example administering mEphA4-Fc every two weeks, every three weeks, or every four weeks, and at a concentration of about 10 to about 40 mg/kg body weight of a subject.
Resumen de: WO2025021908A1
The present invention relates to a composition comprising an estetrol component for use in the prevention and treatment of menopause-associated Alzheimer's disease symptoms. The composition described herein displays favorable properties when compared to existing estrogen-based compositions that aim to alleviate estrogen deficiency symptoms. Also described are related uses and methods of treatment comprising administration of the composition.
Resumen de: EP4751721A1
The present invention relates to a use of a novel compound for preventing, alleviating, or treating Parkinson's disease, the novel compound exhibiting an effect of inhibiting synuclein aggregation in a Parkinson's disease (PD) mouse model. As a result of histological analysis, it was confirmed that the loss of dopaminergic neurons was blocked by treatment with the novel compound. Therefore, the novel compound can be effectively utilized in the development of a therapeutic agent for Parkinson's disease.
Resumen de: MX2026005980A
The invention provides compositions and methods for the treatment of diseases associated with amyloid deposits of Aβ in the brain of a patient, such as Alzheimer's Disease. Such methods entail administering a pharmaceutical composition comprising an immunogenic fragment of Aβ capable of inducing a beneficial immune response in the form of antibodies to Aβ. The immunogenic fragments comprise linear or multivalent peptides of Aβ. Pharmaceutical compositions comprise the immunogenic fragment chemically linked to a carrier molecule which may be administered with an adjuvant.
Resumen de: US20260146249A1
The invention relates to the field of human genetics, more specifically to treatments for a disease or condition associated with an abnormal processing of the Amyloid Precursor Protein (APP), preferably familiar Alzheimer disease (FAD). The invention in particular relates to antisense oligonucleotides (AON's) that can be used for treating such diseases or conditions.
Resumen de: US20260144772A1
Pharmaceutical compositions comprising antioxidants as useful therapeutic agents for treatment of amyotrophic lateral sclerosis (ALS), and methods thereof, are disclosed. In particular, the present disclosure provides enteric capsules and intravenous (i.v.) drip of aspirin-mimetic antioxidant drugs in intervention of ALS.
Resumen de: AU2026203567A1
The invention relates to methods for promoting SCFA production by gut microbiota by administering a liquid, water-based probiotic composition. The methods are particularly effective at promoting gut health. The invention further relates to methods of promoting intestinal barrier integrity, methods of promoting a tolerogenic gut phenotype, and methods 5 of treating Parkinson’s Disease. ay a y
Resumen de: WO2026112645A1
The present disclosure provides novel methods for treatment of patients with autophagy diseases by administering a prodrug of dexibuprofen, such as but not limited to dexibuprofen dimethylamino ethyl ester (mDex) or a pharmaceutically acceptable salt thereof and compositions comprising the same.
Nº publicación: WO2026112233A1 28/05/2026
Solicitante:
MERCK SHARP & DOHME LLC [US]
MERCK SHARP & DOHME LLC
Resumen de: WO2026112233A1
Disclosed are substituted heterocyclic compounds of formula (I) and pharmaceutically acceptable salts thereof, which may be suitable for imaging tau aggregates, b-sheet aggregates, beta-amyloid aggregates or alpha-synuclein aggregates, and hence are useful in binding and imaging tau aggregates in Alzheimer's patients. More specifically, this invention relates to a method of using the compounds of formula (I) as tracers in positron emission tomography (PET) imaging to study tau deposits in brain in vivo to allow diagnosis of Alzheimer's disease and other neurodegenerative diseases characterized by tau pathology. The disclosure further relates to a method of measuring clinical efficacy of therapeutic agents for Alzheimer's disease and other neurodegenerative diseases characterized by tau pathology.