DNA damage or cellular stresses can induce senescence, and increased senescence with aging contributes to age-associated tissue damage, inflammation and disease. Zheng and colleagues report increased senescent oligodendrocyte progenitor cells around amyloid plaques. Therapeutically eliminating these senescent cells may influence the onset and progression of Alzheimer’s disease pathology.

Original languageEnglish
Pages (from-to)683-684
Number of pages2
JournalNature neuroscience
Issue number5
StatePublished - May 1 2019


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