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NEURODEGENERATIVE DISEASE

Senescent glia spell trouble in Alzheimer’s disease

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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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Fig. 1: Senolytic therapy eliminates senescent OPCs, reduces Aβ and attenuates inflammation.

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Authors and Affiliations

  1. Department of Neurology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, USA

    David Holtzman & Jason Ulrich

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  1. David Holtzman
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  2. Jason Ulrich
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Correspondence to David Holtzman.

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The authors declare no competing interests.

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Holtzman, D., Ulrich, J. Senescent glia spell trouble in Alzheimer’s disease. Nat Neurosci 22, 683–684 (2019). https://doi.org/10.1038/s41593-019-0395-2

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