Phagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia.

ABSTRACT: BACKGROUND:Alzheimer's disease is associated with the accumulation of intracellular Tau tangles within neurons and extracellular amyloid-β plaques in the brain parenchyma, which altogether results in synaptic loss and neurodegeneration. Extracellular concentrations of oligomers and aggregated proteins initiate microglial activation and convert their state of synaptic surveillance into a destructive inflammatory state. Although Tau oligomers have fleeting nature, they were shown to mediate neurotoxicity and microglial pro-inflammation. Due to the instability of oligomers, in vitro experiments become challenging, and hence, the stability of the full-length Tau oligomers is a major concern. METHODS:In this study, we have prepared and stabilized hTau40WT oligomers, which were purified by size-

SUBMITTER: Das R 

PROVIDER: S-EPMC6950897 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature