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Alzheimer's disease

High-Content Image-Based Analysis and Proteomic Profiling Identifies Tau Phosphorylation Inhibitors in a Human iPSC-Derived Glutamatergic Neuronal Model of Tauopathy

[Scientific Reports] Scientists used iPSCs from a patient carrying a p.A152T tau variant to create a robust, functional cellular assay system for probing pathophysiological tau accumulation and phosphorylation.

Modeling Sporadic Alzheimer’s Disease in Human Brain Organoids under Serum Exposure

[Advanced Science] Serum-exposed brain organoids are able to recapitulate Alzheimer's disease-like pathologies, including increased amyloid beta aggregates and phosphorylated microtubule-associated tau protein level, synaptic loss, and impaired neural network.

A Novel Orally Active HDAC6 Inhibitor T-518 Shows a Therapeutic Potential for Alzheimer’s Disease and Tauopathy in Mice

[Scientific Reports] Researchers characterized N-[(1R,2R)-2-{3-[5-(difluoromethyl)-1,3,4-oxadiazol-2-yl]-5-oxo-5H,6H,7H-pyrrolo[3,4-b]pyridin-6-yl}cyclohexyl]-2,2,3,3,3-pentafluoropropanamide (T-518), a novel, potent, highly selective histone deacetylase 6 inhibitor with clinically favorable pharmacodynamics.

Apolipoprotein E Promotes Immune Suppression in Pancreatic Cancer through NF-kB-Mediated Production of CXCL1

[Cancer Research] Investigators reported that ApoE was elevated in peripheral blood monocytes in pancreatic ductal adenocarcinoma patients, and plasma ApoE protein levels stratified patient survival.

Overlapping Roles of JIP3 and JIP4 in Promoting Axonal Transport of Lysosomes in Human iPSC-Derived Neurons

[Molecular Biology of the Cell] Investigators established a hiPSC-derived neuron model for the investigation of axonal lysosome transport and maturation and showed that loss of JIP3 resulted in the accumulation of axonal lysosomes and the Alzheimer's disease-related amyloid precursor protein-derived Aβ42 peptide.

Sex Differences in the Blood–Brain Barrier and Neurodegenerative Diseases

[APL Bioengineering] The authors describe sex-related differences in neurodegenerative diseases and the blood–brain barrier, whose dysfunction is linked to neurodegenerative disease development and progression.

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