Different from tau dependent model, D + Q removed senescent OPCs that highly expressed p16 induced by Aβ in short-term treated APP/PS1 mutant AD mice, reduced neuroinflammation and Aβ plaque size, and in the long-term intermittent treatment, it alleviated learning and memory deficits (Zhang et al., 2019). This evidence concerns the gene CDKN2A and Alzheimer disease.