As an essential indicator of AD diagnosis, Aβ starts to aggregate insidiously about 20 years before the presence of any obvious symptoms.1 During this long interval, neuroinflammation is a key driving factor for the AD progression,2 which can be exacerbated by nearly half of the AD risk genes (APOE, TREM2, CD33, etc.)that are implicated in immune processes,3,4 increased levels of complement molecules and inflammatory mediators,5 and the reactive gliosis and infiltration of immune cells in the brain. This evidence concerns the gene CD33 and Alzheimer disease.