The first-generation senolytic ABT263 is able to clear senescent astrocytes and microglia, modulate tau aggregation and inhibit tau-associated cognitive decline.410 Likewise, D + Q senolytic treatment reduced Aβ-related oligodendrocyte senescence, improved cognitive impairments, and decreased Aβ load and neuroinflammation in AD mice.411 In another way, D + Q also decreases cortical Tau‐containing neurofibrillary tangles (NFTs) burden, brain atrophy and neuron damage.412 However, senolytic therapy is rarely reported in treating PD and ALS. The gene discussed is MAPT; the disease is Alzheimer disease.