Analysis of the modulatory effects of amyloid-beta and age on microglial activation

Abstract

Microglia are the resident immune cells of the brain, and in the healthy brain they are believed to be responsible for the clearance of amyloid-beta (Aβ). Age is a primary risk factor for Alzheimer’s disease (AD) and the age-related proinflammatory environment is thought to contribute to the pathogenesis of AD. In AD, activated microglia have been shown to be associated with insoluble Aβ plaques, but whether they play a role in phagocytosis of Aβ in this context is not known. Both inflammatory molecules and Aβ can trigger neurodegenerative changes and both exert a negative impact on memory. Therefore it is believed that both play a crucial role in the pathogenesis of AD.