TLR2 was proposed to act as a receptor for Aβ clearance as TLR2 KO mice overexpressing AD-associated genes for mutated presenilin 1 and amyloid precursor protein (APP) exhibited accelerated memory impairment and increased accumulation of the fibrillary Aβ(1-42) peptide in the brain (81, 82). The gene discussed is APP; the disease is Alzheimer disease.