期刊
NATURE NEUROSCIENCE
卷 22, 期 5, 页码 683-684出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-019-0395-2
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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.
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