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

Alzheimer's disease (AD) is characterized by neuroinflammation, accumulation of amyloid-ß (Aß) 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. Overall design: The aim of the experiment was to find differentially expressed genes between apoE and or FH treated microglial cells in the presence of amyloid-ß 1-42 to understand the role of these proteins in microglial mediated inflammatory responses and amyloid-ß clearance. The experiment was done as three separate experiments using duplicates.