Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease.

ABSTRACT:

Background

Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting memory and cognition. The disease is accompanied by an abnormal deposition of ß-amyloid plaques in the brain that contributes to neurodegeneration and is known to induce glial inflammation. Studies in the APP/PS1 mouse model of ß-amyloid-induced neuropathology have suggested a role for inflammasome activation in ß-amyloid-induced neuroinflammation and neuropathology.

Methods

Here, we evaluated the in vivo role of microglia-selective and full body inflammasome signalling in several mouse models of ß-amyloid-induced AD neuropathology.

Results

Microglia-specific deletion of the inflammasome regulator A20 and inflammasome effector protease caspase-1 in the App

SUBMITTER: Srinivasan S 

PROVIDER: S-EPMC10863058 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature