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

Table 1

Outline of microglia receptors and their function in Alzheimer’s disease.

Microglia receptors	Functions in Alzheimer’s disease	References
Complement receptors (CRs)	(i) Phagocytic uptake; (ii) Microglia activation; (iii) Proinflammatory molecule generation; (iv) Aβ clearance	[89–92, 94–97]
Toll-like receptors (TLRs)	(i) Proinflammatory mediator generation; (ii) Aβ clearance; (iii) Microglia activation; (iv) Synaptic plasticity; (v) tau phosphorylation	[15, 98–103]
Scavenger receptor type-A (SR-A)	(i) Aβ internalization and clearance; (ii) Inflammatory response; (iii) Maintain microglia immune response	[104–107]
Cluster of differentiation 36 (CD36)	(i) Microglia recruitment; (ii) Inflammatory response; (iii) Activation of Aβ phagocytosis; (iv) Modulates microglial Aβ42 phagocytosis	[108–111]
Receptor for advanced glycation end products (RAGE)	(i) Microglia activation; (ii) Stimulate IL-1β; (iii) TNF-α production; (iv) Intensify oxidative stress	[112–116]
Triggering receptor expressed in the myeloid cell 2 (TREM2)	(i) Aβ clearance; (ii) Regulates microglial mammalian target of rapamycin (mTOR) activation and metabolism; (iii) Balanced microglial autophagy	[117, 118]