Interestingly, the authors showed that CD22 was a negative regulator of microglial phagocytosis, and blocking CD22 in CNS either by specific antibody or by genetic ablation promoted the clearance of extracellular oligomeric amyloid-β [Aβ, neuropathological hallmark of Alzheimer's disease (AD)] and α-synuclein fibrils (pathological hallmark of Parkinson's disease) in vivo, and improved hippocampal-dependent learning and memory performance. This evidence concerns the gene CD22 and Alzheimer disease.