Oxidative stress has long been considered to contribute to brain aging and age-related neurodegenerative disorders including Parkinson’s and Alzheimer’s disease¹.  Data over the last few years suggests that one important mechanism driving neuropathology associated with these disorders is a process known as cellular senescence. In response to stressors including agents which elicit oxidative or proteotoxic stress, cells may undergo conversion to a resting state where they are not capable of replicating and forming tumors. However, maintenance of these cells over long periods of time in the aging organism can result in increased inflammatory events known as the senescent associated secretory phenotype or SASP which is damaging to neighboring tissues, including within the brain. Here, I will present data suggesting that not only does cellular senescence occur in conjunction with age-related neurodegenerative diseases, but that elimination of senescent cells may constitute a therapeutic avenue for these disorders^2-4. This is dependent however on selectivity of senescent cell removal which avoids off-target effects on other cell types.