In the APP/PS1 model of Alzheimer's disease OPCs expressing upregulated p16, p21, and senescence-associated-β-Galactosidase (SA-β-Gal) markers of CS have been identified in association with Aβ plaques and treatments aiming to remove senescent OPCs (senolytics) attenuated neuroinflammation and cognitive deficits, indicating that OPC SASP promotes neuroinflammation and functional impairment (Zhang et al., 2019). The gene discussed is CDKN2A; the disease is Alzheimer disease.