Figure 2.

Possible mechanisms underlying microglial activation Aβ deposition and subsequent pro-inflammatory cytokine release contribute to AD. In the early stages of AD microglial activation can promote Aβ clearance via microglia’s SRs. The persistent microglial activation stimulated by Aβ via the receptor for CD36, Fc receptors, TLRs and RAGE, creating a vicious circle between microglia activation, neuroinflammation, and Aβ accumulation. A crucial role on pathogenesis of AD is an absolute culprit for both amyloid plaque and other pathologic change such as the neuronal damage. Aβ, amyloid-β; AD, Alzheimer’s disease; SRs, scavenger receptors; TLRs, toll-like receptors; RAGE, complement receptors advanced glycation end products; NO, nitric oxide; ROS, reactive oxygen species.