IPLA2β loss leads to age-related cognitive decline and neuroinflammation by disrupting neuronal mitophagy.

ABSTRACT:

Background

During brain aging, disturbances in neuronal phospholipid metabolism result in impaired cognitive function and dysregulation of neurological processes. Mutations in iPLA2β are associated with neurodegenerative conditions that significantly impact brain phospholipids. iPLA2β deficiency exacerbates mitochondrial dysfunction and abnormal mitochondrial accumulation. We hypothesized that iPLA2β contributes to age-related cognitive decline by disrupting neuronal mitophagy.

Methodology

We used aged wild-type (WT) mice and iPLA2β^-/- mice as natural aging models to assess cognitive performance, iPLA2β expression in the cortex, levels of chemokines and inflammatory cytokines, and mitochondrial dysfunction, with a specific focus on mitophagy and the mitochondrial

SUBMITTER: Jiao L 

PROVIDER: S-EPMC11409585 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature