Abstract

Beta-Amyloid (Abeta) aggregates are reputed to play a central role in AD pathogenesis, partly by triggering neuroinflammation. Peripheral monocytes can shift into the CNS, hence participating in Abeta oligomer clearance. Donepezil's anti-AD mechanism remains largely elusive; however, it can interact with monocyte α7nAChR that is involved in Abeta phagocytosis. We believe that by binding to α7nAChR, Donepezil can modulate Abeta internalization driven by both α7nAChR and TREM2.

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