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Obesity-Induced Cellular Senescence Drives Anxiety and Impairs Neurogenesis.

Cell metabolism | 2019

Cellular senescence entails a stable cell-cycle arrest and a pro-inflammatory secretory phenotype, which contributes to aging and age-related diseases. Obesity is associated with increased senescent cell burden and neuropsychiatric disorders, including anxiety and depression. To investigate the role of senescence in obesity-related neuropsychiatric dysfunction, we used the INK-ATTAC mouse model, from which p16-expressing senescent cells can be eliminated, and senolytic drugs dasatinib and quercetin. We found that obesity results in the accumulation of senescent glial cells in proximity to the lateral ventricle, a region in which adult neurogenesis occurs. Furthermore, senescent glial cells exhibit excessive fat deposits, a phenotype we termed "accumulation of lipids in senescence." Clearing senescent cells from high fat-fed or leptin receptor-deficient obese mice restored neurogenesis and alleviated anxiety-related behavior. Our study provides proof-of-concept evidence that senescent cells are major contributors to obesity-induced anxiety and that senolytics are a potential new therapeutic avenue for treating neuropsychiatric disorders.

Pubmed ID: 30612898 RIS Download

Associated grants

  • Agency: Biotechnology and Biological Sciences Research Council, United Kingdom
    Id: BB/H022384/1
  • Agency: NIA NIH HHS, United States
    Id: R37 AG013925
  • Agency: Biotechnology and Biological Sciences Research Council, United Kingdom
    Id: BB/F010966/1
  • Agency: Biotechnology and Biological Sciences Research Council, United Kingdom
    Id: BB/I020748/1
  • Agency: NIA NIH HHS, United States
    Id: R01 AG013925
  • Agency: Medical Research Council, United Kingdom
    Id: MR/L016354/1

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