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Dysfunction of pyramidal neuron-PV interneuron circuits contributes to cognitive failure in Alzheimer's disease.

A protein called NPTX2 may be a useful marker of neural circuit defects in patients with Alzheimer's disease.

Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.

Solution NMR provides structural and kinetic information about oligomers on pathway to amyloid fibrils that are precisely structured but not cytotoxic.

Genome-wide CRISPRi screens and proteome profiling of lysosomes link lipid dysregulation to ESCRT disruption and proteostasis defect.

APPPS1 microglia express disease-associated proteomic signatures of Alzheimer's disease earlier, compared to the APP-KI, and these differences correlate with the levels of fibrillar Aβ and impaired microglial phagocytic function.

Tau proteins can convert from an inert shape to a misfolded shape that seeds the growth of fibers that contribute to the pathology of Alzheimer's disease.

Mutated NLRP3 forms cryo-sensitive aggregates that induce inflammasome assembly distinct from the canonical NLRP3 inflammasome.