As evidenced by their increased SA-βgal expression, p53 expression, a mediator of cellular senescence, an increase in the release of SASP components, DNA damage, telomere attrition or damage, and senescence-like morphological changes, increased senescence is found in various cell types of AD brains, including astrocytes, microglia, and neurons (Caldeira et al., 2017). This evidence concerns the gene TP53 and Alzheimer disease.