Reduced binding of apoE4 to complement factor H promotes amyloid-β oligomerization and neuroinflammation

Alzheimer’s disease (AD) is characterized by neuroinflammation, accumulation of amyloid-β (Aβ) plaques and neuronal degeneration in the brain. The APOE4 variant of apolipoprotein E (apoE) is the most prevalent genetic risk allele associated with late-onset AD. ApoE interacts with complement regulator factor H (FH) but the role of this interaction in AD pathogenesis is unknown. The aim of the experiment was to find differentially expressed genes between apoE and or FH treated microglial cells in the presence of amyloid-β 1-42 to understand the role of these proteins in microglial mediated inflammatory responses and amyloid-β clearance. The experiment was done as three separate experiments using duplicates.