Researchers at INSERM and collaborators have identified hypothalamic tanycytes as mediators of tau clearance and shown that their structural and genetic disruption may drive Alzheimer’s disease pathology.
Researchers at INSERM and collaborators have identified hypothalamic tanycytes as mediators of tau clearance and shown that their structural and genetic disruption may drive Alzheimer’s disease (AD) pathology. AD is characterized by the buildup of extracellular amyloid-β plaques and intracellular tau tangles, protein aggregates that disrupt neuronal function and drive neurodegeneration.
Porosome Therapeutics Inc. has announced the development of novel first-in-class porosome-targeting small molecules and blood-brain barrier-traversing peptide drugs developed using the company’s Porosome.AI platform to treat various secretory disorders, such as Alzheimer’s disease and type 2 diabetes.
Korsana Biosciences Inc. has emerged from stealth, with its development of therapeutics to treat neurodegenerative diseases initially focused on Alzheimer’s disease.
Building on the foundation laid in 2020, researchers at the University of California, San Francisco (UCSF) have now shown that targeting the GPI-anchored vascular enzyme TNAP can reproduce the cognitive benefits previously attributed to the liver-derived exercise factor GLPD1.
Tau is an intrinsically disordered protein that regulates the stability and dynamics of microtubules in physiological conditions. Recent work has revealed the involvement of tau in various neuronal processes. Researchers from the University of California and collaborators aimed to systematically investigate the cellular factors that control the accumulation of tau aggregates in human neurons.
Aquinnah Pharmaceuticals Inc. has disclosed new microtubule-associated protein τ (PHF-τ; MAPT) aggregation inhibitors designed for use in the treatment of Alzheimer’s disease and frontotemporal dementia.
Researchers from the Medical University of South Carolina report the development of novel genetic mouse models that enable pericyte chemogenetic modulation, which could reduce neuronal damage and cognitive decline in Alzheimer’s disease.
Researchers from the University of Oxford and the Health Research Institute La Fe (Spain) investigated the potential of multigene RNA-based therapeutics in Alzheimer’s disease, aiming to overcome potential compensatory mechanisms and patient heterogeneity.
The serine/threonine kinase glycogen synthase kinase-3β (GSK-3β) plays a multifunctional role through its involvement in multiple signaling pathways. Because of its relevant role in Alzheimer’s disease (AD) pathogenesis, regulating GSK-3β activity has been proposed as a potential approach to target AD-related pathology.
