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Different senescent cell populations secrete senescence-associated secretory phenotypes (SASP), including matrix metalloproteinase-3, interleukin (IL)-1\u03b1, IL-6, and IL-8, which can harm adjacent microglia. Moreover, these cells possess high expression levels of senescence hallmarks (p16 and p21) and elevated senescence-associated \u03b2-galactosidase activity in in vitro and in vivo ND models. These senescence phenotypes contribute to the deposition of \u03b2-amyloid and tau-protein tangles. Selective clearance of senescent cells and SASP regulation by inhibiting p38\/mitogen-activated protein kinase and nuclear factor kappa B signaling attenuate \u03b2-amyloid load and prevent tau-protein tangle deposition, thereby improving cognitive performance in AD mouse models. In addition, telomere shortening, a cellular senescence biomarker, is associated with increased ND risks. Telomere dysfunction causes cellular senescence, stimulating IL-6, tumor necrosis factor-\u03b1, and IL-1\u03b2 secretions. The forced expression of telomerase activators prevents cellular senescence, yielding considerable neuroprotective effects. 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