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165
results.
Updated on
19/04/2026 [07:25:00]
Absstract of: WO2026078185A1
The present invention relates to a composition comprising a c-AMP Response Element-Binding protein 3 (CREB3), in particular a variant of CREB3 protein, or a nucleic acid molecule encoding said CREB3 protein or said variant of CREB3 protein, for use as a medicament, in particular for treating or preventing diseases associated with a degeneration of motor neurons. The present invention further relates to CREB3 protein, in particular said variant of CREB3 protein, as a biomarker for the stratification or the prognosis of patients suffering, or susceptible of suffering, from a disease associated with a degeneration of motor neurons.
Absstract of: WO2026080811A1
Provided are methods and compositions for treating Parkinson's disease (PD). The compositions inhibit the expression or activity of adenosylmethionine decarboxylase 1 (AMD1).
Absstract of: WO2026076481A1
The present disclosure related generally to polynucleotide sequences encoding an antigen-binding construct capable of specifically binding to intracellular tau, and uses thereof, in particular for the treatment of tauopathies, including Alzheimer's Disease.
Absstract of: WO2026077862A1
The application relates to fused pyrimidinone derivatives of the general formula (I) which act as agonists of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) useful for the treatment of Parkinson's disease, rheumatoid arthritis, Alzheimer's disease, amyotrophic lateral sclerosis, Nasu-Hakola disease, frontotemporal dementia, multiple sclerosis, prion disease, and stroke.
Absstract of: WO2026077861A1
The application relates to fused pyrimidinone derivatives of the general formula (I) which act as agonists of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) useful for the treatment of Parkinson's disease, rheumatoid arthritis, Alzheimer's disease, amyotrophic lateral sclerosis, Nasu-Hakola disease, frontotemporal dementia, multiple sclerosis, prion disease, and stroke.
Absstract of: WO2026076634A1
Provided are Aβ375 related oligomers/aggregates in human brains and anti-Aβ3175 related oligomers/aggregates antibodies thereof. In addition, the using of anti-Aβ3175 related oligomers/aggregates antibodies for the treatment of Alzheimer's disease (AD) is also provided.
Absstract of: WO2026079761A1
The present invention relates to a composition for alleviating, preventing, or treating Alzheimer's disease, the composition comprising apigenin and oxyresveratrol. A composition according to the present invention is highly effective in reducing Alzheimer's disease pathology caused by β-amyloid, which is increased by aging and oxidative stress, and improving β-amyloid-induced memory loss and cognitive function.
Absstract of: WO2026080717A1
Methods and compositions for treating or reducing the development of neurodegenerative diseases.
Absstract of: WO2026077192A1
Provided in the present invention are preparation and use of a novel MAO-B inhibitor containing a tetralin-1-amine structure, which belong to the field of medicines. The derivative is a compound represented by formula I, or a pharmaceutically acceptable salt thereof, or a stereoisomer thereof. The compound of the present invention can be used for inhibiting monoamine oxidase (MAO), especially selectively inhibiting MAO-B. The compound can be used for treating diseases such as Parkinson's disease, Alzheimer's disease, and emotional disorders, and exhibits good application prospects.
Absstract of: WO2026077393A1
The present invention belongs to the field of biopharmaceuticals. Disclosed are a Muse cell-derived protein complex, a preparation method therefor, and use thereof. The composition of the protein complex is: a stem cell lysate of Muse cells after being cultured in a stress environment for a predetermined time, or a protein complex obtained by separating and purifying the stem cell lysate. The protein complex has a good cell damage repair effect, especially a strong ability to repair nerve cell damage, and is expected to be used for treating neurodegenerative diseases, cerebral stroke, cerebrovascular disease, arthritis, enteritis, recovery after trauma, autism, depression, and pulmonary fibrosis. In particular, the neurodegenerative diseases include, but are not limited to, Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and different types of spinocerebellar ataxia (SCA).
Absstract of: WO2026077305A1
Provided are a method and a drug combination for preventing or treating neurodegenerative diseases, comprising a pharmaceutical composition and a combination drug product. The drug combination, the pharmaceutical composition, and the combination drug product can be used to treat and/or prevent neurodegenerative diseases in patients, preferably neurodegenerative diseases associated with α-synuclein aggregation, and more preferably Parkinson's disease.
Absstract of: AU2024354107A1
Provided are an siRNA inhibiting the expression of an amyloid precursor protein (APP) gene in a human cell, a polypeptide-oligonucleotide drug, and a use. The siRNA has good APP expression inhibitory activity, and a suitable modification is made to the siRNA to improve the silencing capability against a target and reduce off-target activity. The siRNA and a conjugate thereof are expected to be applied for clinically preventing and treating an APP target-related disease such as cerebral amyloid angiopathy (CAA), early-onset familial Alzheimer's disease (EOFAD), or Alzheimer's disease (AD).
Absstract of: WO2026077485A1
The present invention relates to an application of a DFNA5/GSDME inhibitor in preparing a drug for treating Alzheimer's disease. Also provided is an application of a specific DFNA5 gene knockdown system in preparing a drug for treating Alzheimer's disease. The present invention demonstrates that in reactive astrocytes of patients with Alzheimer's disease, the mRNA expression level of GSDME is significantly high, and GSDME can be used as an effective target for Alzheimer's disease. Provided is an application of a reagent, which specifically inhibits GSDME gene expression in astrocytes, in preparing a drug for treating Alzheimer's disease, so as to develop a novel treatment drug for Alzheimer's disease. The present invention demonstrates that the reagent, which inhibits GSDME gene expression, can be used for preparing a drug for treating Alzheimer's disease. The present invention also provides a theoretical basis for clinical treatment of Alzheimer's disease.
Absstract of: EP4725506A2
The present disclosure provides novel methods for treating or preventing amyotrophic lateral sclerosis (ALS), methods for delaying the onset of neurological symptoms associated with ALS, increasing survival in subjects afflicted with ALS, and attenuating the decline of muscle strength associated with ALS in a subject in need thereof. The present disclosure also provides methods for treating or preventing α-synucleinopathy or TDP-43 proteinopathy. The methods comprise administering to the subject an effective amount of a mitochondriatargeting peptidomimetic compound, such as (R)-2-amino-N-((S)-1-(((S)-5-amino-1-(3-benzyl-1,2,4-oxadiazol-5-yl)pentyl)amino)-3-(4-hydroxy-2,6-dimethylphenyl)-1-oxopropan-2-yl)-5-guanidinopentanamide, or a pharmaceutically acceptable salt, stereoisomer, tautomer, hydrate, and/or solvate thereof.
Absstract of: EP4725499A1
The present invention is related to the biomedical and biopharmaceutical sectors. Specifically, it refers to a chimeric antigen comprising the combination of the amino and carboxyl terminal regions of the amyloid beta peptide (Aβ), the amino and carboxyl terminal regions of the tau protein and a T cell epitope. The pharmaceutical composition comprising this chimeric antigen and at least one pharmaceutically acceptable vaccine adjuvant increases the efficacy of immunotherapy for the prevention and treatment of Alzheimer's Disease (AD). The chimeric antigen exerts its action by stimulating a multitarget humoral response with high titers of anti-Aβ and anti-tau antibodies simultaneously. This favors the combined elimination of toxic species of both Aβ and tau from the brain, which prevents or significantly improves the clinical symptoms and neuropathology of AD.
Absstract of: EP4725497A1
The present invention relates to a pharmaceutical composition for use in preventing or treating periodontal disease, or atherosclerosis or Alzheimer's disease caused by periodontal disease, more particularly, a pharmaceutical composition comprising a peptide having the amino acid sequence of SEQ ID NO: 1 to prevent or treat the periodontal disease or the atherosclerosis or Alzheimer's disease caused by periodontal disease, so that it is effective in suppressing osteoclastogenesis, suppressing Porphyromonas gingivalis colony formation, and suppressing gingipain expression. Further, the pharmaceutical composition is safe to a living body and involves less side effects including abnormal response.
Absstract of: EP4725321A1
0001 The present invention provides a medical food composition comprising at least one probiotic and optionally one or more amino acids. The composition is useful in patients with Parkinson's disease to enhance the systemic stability and central bioavailability of levodopa (L-DOPA). It exerts effects by modulating gut microbiota, reinforcing intestinal barrier integrity, and reducing systemic inflammation and oxidative stress, thereby improving motor and non-motor symptoms and minimizing L-DOPA-induced long-term side effects such as dyskinesia.
Absstract of: EP4725322A1
The present invention relates to a probiotic cocktail medical food composition and its use in delaying the progression of Parkinson's disease. The composition comprises: (a) at least one probiotic with neuroprotective or metabolic regulatory functions; (b) a functional amino acid combination comprising four or more essential amino acids. The composition can be formulated as a medical food product for improving or alleviating pathological conditions associated with Parkinson's disease, including motor dysfunction, cognitive decline, inflammation, and mitochondrial impairment. It is suitable for daily nutritional supplementation and disease progression delay in patients with Parkinson's disease or individuals at high risk.
Absstract of: US20260097090A1
The present application provides methods of treating a neurodegenerative disease (such as Alzheimer's disease) in patients by use of a herbal extract composition that has an extract from a mixture including Ophiopogon japonicus, Barbary Wolfberry, Rhizoma Acori tatarinowii and Codonopsis pilosula. Compositions having such extract and the methods of preparing such a composition are also contemplated.
Absstract of: WO2026075947A1
The invention pertains to a method for reducing amyloid plaques in the brain of a human suffering from a disease characterized by Aβ plaques in the brain, e.g., Alzheimer's disease. The invention also relates to a method for preventing or reducing amyloid plaques in the brain of a primary prevention subject. Certain aspects of the invention involve methods, doses, or dosing regimens that decrease the risk, frequency, severity, or occurrence of ARIA in subjects.
Absstract of: WO2026074007A1
The present relates to novel nuclear receptor related 1 (Nurr1) modulators, preferably agonists, having a new carboxylic acid/carboxamide bioisosteric moiety Y and being optionally deuterated, pharmaceutical formulations comprising them, a process for their preparation and their use as medicament, alone or in combination with one or more additional agents, for treating of various diseases, wherein the modulation of Nurr1 is beneficial in such diseases (e.g. multiple sclerosis or Parkinson's disease).
Absstract of: US20260097130A1
The present invention provides a method of treating neurodegenerative diseases. The method comprises the step of administering to a subject in need thereof an effective amount of a polymer-flavonoid conjugate, or a nanocomplex having an outer shell comprising one or more polymer-flavonoid conjugates and optionally an inner shell comprising one or more flavonoid oligomer and a drug such as anti-CD3 or anti-CD33 encapsulated within the shells. The present method brings therapeutic effective materials through blood-brain barrier to treat neurodegenerative diseases. The present method is effective to treat neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Lewy body dementia and Huntington's disease.
Absstract of: AU2024334482A1
Disclosed are novel strategies for the treatment of patients with Parkinson's disease and other secondary Parkinsonian disorders. Disclosed are DA neuronal cells that have been modified in vitro with a genetic insertion of GDNF. The GDNF coding sequence is inserted under the transcriptional control of a promotor such that secreted proteins are made and taken up by the endogenous cells after the administered engineered cells have matured to a Neuronal Mature Cell Type to promote survival of endogenous neurons. Also disclosed are DA neuronal cells that have been modified with a genetic insertion of GBA in vitro and are hemizygous null for SNCA. The GBA coding sequence is inserted under the transcriptional control of a ubiquitous promotor and the secreted proteins are made and taken up by the graft and endogenous cells immediately upon transplantation to promote long-term graft integrity.
Absstract of: US20260098038A1
Provided are a compound having a 2,3-dihydro-1H-indene or 2,3-dihydrobenzofuran moiety or pharmaceutically acceptable salt thereof, a process for the preparation thereof, a pharmaceutical composition comprising the same and a use thereof, where the. The compound having a 2,3-dihydro-1H-indene or 2,3-dihydrobenzofuran moiety or pharmaceutically acceptable salt thereof has an inhibitory activity against glucosylceramide synthase (GCS), and therefore can be usefully applied for preventing or treating various diseases associated with GCS, such as Gaucher disease, Fabry disease, Tay-Sachs disease, Parkinson's disease, etc.
Nº publicación: US20260098268A1 09/04/2026
Applicant:
THE BOARD OF REGENTS OF THE UNIV OF TEXAS SYSTEM [US]
Absstract of: US20260098268A1
0000 Pharmacological or genetic inactivation of MAGL reduces neuroinflammation and neuropathology in animal models of AD. However, global inactivation of MAGL induces functional tolerance of CB IR, which reduces the effectiveness of pharmacotherapies. Evidence has shown that selective inactivation of MAGL in astrocytes, but not in neurons, reduces neuropathology and synaptic and cognitive impairments in TBI. In particular, results showed that inactivation of astrocytic MAGL attenuates AD neuropathology and prevents deterioration in LTP, spatial learning and memory in AD animals. This shows that neuroprotective effects of global MAGL inactivation largely result from limiting 2-AG degradation in astrocytes, rather than in neurons. Therefore, selective inactivation of astrocytic MAGL provides a better therapeutic outcome for AD, as this greatly minimizes the potential adverse effects resulting from global inactivation-induced disruption of 2-AG degradation in neurons and in other peripheral tissues. To this end, an AAV-mediated gene silencing approach to knock MAGL selectively in astrocytes is presented.
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