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  • 9 years ago

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  • 01:08:19

Judith Campisi, Ph.D. on Cellular Senescence, Mitochondrial Dysfunction, Cancer & Aging

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Dr. Judith Campisi is a professor of biogerentology at the Buck Institute for Research on Aging and a co-editor in chief of the Aging Journal.

As an expert on cellular senescence, the discussion involves a lot of talk about aging and cancer, where senescence plays a very important fundamental role. What are some of the strategies we might use in the future to prevent senescent cells? What causes them in the first place?

In this 1-hour long conversation, we discuss a great number of very interesting things including:

  • Why diseases of aging, despite occurring in vary diverse tissue types, all begin to crop up simultaneously after 50 or 60 years of life.
  • What the fundamental molecular processes of aging are and what some of the on-going research and general thoughts are surrounding these processes.
  • What senescence is and the evolutionary biology explanation for why we have the mechanism of cellular senescence in the first place.
  • The infiltration of immune cells into our tissues that occurs as a function of aging and the role of damaged or senescent cells in attracting these immune cells.
  • The changes in gut permeability that happens with age and how that may increase our susceptibility to chronic, low-level inflammation.
  • The role of senescent cells in cancer metastasis and progression.
  • The clearance of senescent cells as a valid life extension strategy.
  • How mitochondrial dysfunction, even in the absence of DNA damage, can cause cells to undergo senescence.
  • The interesting observation that senescence from damage versus energy crisis (failed mitochondria) demonstrates a different and unique phenotype of cellular senescence.
  • The effects prolonged fasting may have on the clearance of senescent cells.
  • How periodic prolonged fasts might mimic some of the effects associated with an mTOR dampening drug like rapamycin.
  • How the secretions of senescent cells can affect the regenerative capacity of stem cells.
  • The practicality of a consumer available clinical assays for DNA damage and the challenge of assessing tissue-specific senescence without the use of invasive biopsy.
  • The effect of so-called fasting mimetic compounds (e.g. hydroxycitrate, resveratrol & spermidine) on senescent cells.
  • And believe it or not much more!

Studies mentioned: 1, 2, 3, 4, 5, 6, 7, 8,


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