A Cell Surface Receptor Complex for Fibrillar β-Amyloid Mediates Microglial Activation

By M. E. Bamberger, Meera E Harris, Douglas R. McDonald, J. Husemann, G. Landreth. Journal of Neuroscience, 2003

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CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior (2009, background): “Several CD36 functions require integrins, and both β2 (28, 57) and β3 (117) integrins coimmunoprecipitated with CD36.”
Alzheimer’s disease: pathogenesis, diagnostics, and therapeutics (2019, background): “In AD, microglia can bind to Aβ via cell-surface receptors, including SCARA1, CD36, CD14, α6β1 integrin, CD47, and Toll-like receptors.(51,52) Following receptor binding, microglia endocytose Aβ oligomers and NFT fibrils, which are eliminated by endolysosomal degrada-”
The role of microglia in amyloid clearance from the AD brain (2010, background): “Blocking TLRs signaling by interfering with receptor–ligand interaction or their downstream effectors also reduced fAb-induced phagocytosis and signaling (Bamberger et al. 2003; Koenigsknecht and Landreth 2004).”
Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease. (2015, background): “The persistent microglial activation stimulated by Aβ via the receptor for CD36 (24), Fc receptors, toll-like receptors (TLRs) (25), and complement receptors advanced glycation end products (RAGE) (26), can increase Aβ production and decrease Aβ clearance, ultimately cause neuronal damage.”