Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by Aβ_1-42 oligomers.

ABSTRACT:

Background

Alzheimer's disease (AD) features progressive neurodegeneration and microglial activation that results in dementia and cognitive decline. The release of soluble amyloid (Aβ) oligomers into the extracellular space is an early feature of AD pathology. This can promote excitotoxicity and microglial activation. Microglia can adopt several activation states with various functional outcomes. Protective microglial activation states have been identified in response to Aβ plaque pathology in vivo. However, the role of microglia and immune mediators in neurotoxicity induced by soluble Aβ oligomers is unclear. Further, there remains a need to identify druggable molecular targets that promote protective microglial states to slow or prevent the progression of AD.

Methods

Hippo

SUBMITTER: Zou J 

PROVIDER: S-EPMC11367981 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature