Microglia in Alzheimer’s Disease: A Favorable Cellular Target to Ameliorate Alzheimer’s Pathogenesis

Figure 2

The linkage of microglia receptors in the pathogenesis of Alzheimer’s disease. CR3 is responsible for the Aβ-induced microglial activation and involved in Aβ-mediated microglia free radical generation as well as uptake and clearance of Aβ. TLR2 is implicated in the generation of the inflammatory response. On the other hand, TLR4 (i.e., stimulated with LPS) is associated with the clearance of Aβ. Microglia cells showed an increase in Aβ uptake. The binding of Aβ to SRs internalizes Aβ and could activate inflammation responses and generate reactive species. Microglia RAGE-Aβ interaction triggers the genesis of proinflammatory molecules that causes neuronal destruction. PM: plasma membrane; Aβ: amyloid beta; CR: complement receptor; LPS: lipopolysaccharide; TLR: Toll-like receptor; SR: scavenger receptor; RAGE: receptor for advanced glycation end products; ROS: reactive oxygen species.