Judith Campisi, PhD

Professor, The Buck Institute

In Conversation: May 14, 2019 | 3pm est/12pm pst

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Join Dr. Judith Campisi live May 14th from the Buck Institute, as she shares her perspectives on the tremendous advancements in biological understanding achieved in the last 30 years.

Dr. Campisi received her PhD from the State University of New York, and postdoctoral training at Harvard Medical School. She was on the Boston University Medical School faculty before joining Lawrence Berkeley National Laboratory in 1991.

Dr. Campisi came to the Buck in 2002 where she embarked on a broad program to understand the relationship between aging and disease, with an emphasis on cancer and aging. Her laboratory has made pioneering discoveries in the field of cellular senescence, and she has received numerous awards for her research. Dr. Campisi is a scientific co-founder of Unity Biotechnology. She is a member of the National Academy of Sciences.

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In her upcoming session, Dr. Campisi will respond to the five questions registered attendees want answered most.

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  • 5

    votes

    In your presentation at Undoing Aging conference, on last March in Berlin, you said that, as repeated senolytics treatment in mouses improved healthspan and lifespan but didn’t improved maximum lifespan, it seemed to mean that evolution was wanting “to say something to us”, what I understood that it could be an evolutionary reason to the maximum lifespan be practically fixed in a species. However, there could be another explanation, that is that, as Aubrey de Grey explains in the book Ending Aging, also for evolutionary reasons, all the fundamental damages of aging (in the case of de Grey’s proposition, seven) occur relatively at the same time, so if all the seven types of damage are not repaired, we can only buy time and health until the usual maximum lifespan of the species be reached, especially in a complex species like humans. Do you think this is a valid explanation for the fact that the mouses couldn’t increase their maximum lifespan with repeated senolytics treatment?

  • 4

    votes

    Unfortunately, in some cases, removal of old cells by senolytic does not lead to the replacement of losses by new functional cells. Are you planning to develop ways to activate the proliferation or reprogramming of neighboring cells in situ? For example, using Fgf10 for stimulation (https://doi.org/10.1016/j.stemcr.2019.04.003) or by conditional immortalization using small molecules (ROCK inhibitors and / or p53 isoforms)?

  • 4

    votes

    Can you list in order of importance science and Biotech companies should be working on the 7 Hallmarks of aging?

  • 4

    votes

    Do you believe that the immune system can be improved to knock out chronic senescent cells more in our older age by improving the microbiome in our gut, skin, nose, etc?

  • 3

    votes

    What are your thoughts of replacing the Thymus gland ever so often to improve the effectiveness of our immune cells to take out accumulating chronic sencesent cells?

  • 3

    votes

    If Senolytics are consumed at a faster rate to keep molecular damage under a certain threshold, can’t the maximum life span be increased? If not, is it due to the fact only 1 of the 7 Hallmarks of aging is being addressed?

  • 2

    votes

    What projects are you and your team currently working on?

  • 2

    votes

    Do you believe that visceral fat cells post the greatest risk of senescent cells on healthspan as many people suffer from overweight and diabetes? Should Senolytics be first programmed to take care of visceral cells?

  • 2

    votes

    Any thoughts on what strategies can be used to break down glucosepane crosslinks in the extracellular matrix?

  • 2

    votes

    How is it going with the following studies after MiDAS? Did you find additional links of mitochondria as a major player in the distinct SASP?

  • 2

    votes

    What is mechanism of molecular action of senolytics? Wouldn’t senolytics also kill quiescent cells (which is really not a good idea) besides killing senescent cells?

  • 2

    votes

    Other than in wound healing, are there any known benefits to the presence of senescent cells? (PS: you’re my fave researcher)

  • 2

    votes

    What’s the status of Unity Biotechnology and senolytic drugs?

  • 2

    votes

    Does senescence play a role in neurodegenerative diseases such as Alzheimer’s and Parkinsons?

  • 2

    votes

    When and how did you realize that senescence was a major player in aging?

  • 1

    votes

    How does senescence drive age-related disease?

  • 1

    votes

    With humans being a higher level of complex species, if all 7 Hallmarks of aging repair are implemented will there be a higher probability of significantly increasing maximum lifespan?

  • 1

    votes

    How has being at the Buck Institute advanced your research?

  • 1

    votes

    Could the biology of aging be akin to a machine fastener that loses its torque over time causing delitourous effects? And just like a fastener, if we apply loctite to the bolt it prevents it from loosening (entropy). Could we identify ways to do the same thing by placing loctite on the P16 gene from activating?

  • 1

    votes

    Does larger short burst stress on the cells activate the P53 gene more to send cells that are reaching the Hayflick limit into apoptosis and smaller longer stress activate the P16 gene to send more cells into senescent? And if so, is that why larger doses of Fisetin back to back works better to knock of senescent cells?

  • 1

    votes

    Have you and your team worked on methods to make copies of the remaining mtDNA to store them in the nucleus where it is safe from mitochondria damage?

  • 1

    votes

    If scientist are successful of repairing the 7 Hallmarks of Aging, do you believe other viruses will rise to the top of the Pareto chart for the new top causes of causes for mortality? That is say preventing human lifespan to reach 200 years old?

  • 1

    votes

    What are your thoughts about increasing NAD+ via NMN? Are humans ready to start consuming this product or do we need to be careful it won’t cause cancer if it’s not highly calibrated dosed and timed?

  • 1

    votes

    What are your thoughts on Induced Pluripontent Stem Cells to reprogram cells that Dr. Yamanaka developed to address the 7 Hallmarks of Aging?

  • 0

    votes

    If senolytics were optimized tomorrow, what would be the next good anti aging target in the SENS list of 7 damage targets?

  • 0

    votes

    If you could name 3 key questions research should address in the forthcoming years, in order to maximise the potential of senolytics, what would these be?

  • 0

    votes

    Are you investigating supplements like Fisetin, Quercetin and Curcumin as senolytics. Is there a possibility that drugs might not be necessary? Since senolytic drugs will only be approved for existing conditions, a population that is not sick might not necessarily have access to these. Not because they don’t need it but because it is the system we have in place. For that reason alone, I am not too hopeful the majority of the population will benefit from these.