George M. Martin, MD
Professor Emeritus, University of Washington
In Conversation: April 16, 2019 | 3pm est/12pm pst
Join Dr. George M. Martin live on April 16 from the University of Washington, as he shares his perspectives on the tremendous advancements in biological understanding achieved in the last 30 years.
Dr. Martin received his BS and MD degrees from the University of Washington and has been a member of its faculty since 1957. His research has centered on genetic approaches to the study of aging and age-related diseases, with a focus on what he has characterized as segmental progeroid syndromes, virtually all of which were shown to support a major role for genomic instability as a fundamental mechanism of aging.
Dr. Martin has received countless honors for his research and election to the National Academy of Medicine. He has also served as president of the Tissue Culture Association, the Gerontological Association of America, and the American Federation for Aging Research.
“We don’t want to just do lifespan. The period of your lifespan that’s healthy: That’s where the action should be.”
Help shape the upcoming conversation.
In his upcoming session, George Martin will respond to the five questions registered attendees want answered most.
You can help shape the upcoming conversation by checking out the list of attendee-requested questions below, and then voting to support the ones that match your own interest.
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What is epigenetics and how does it influence health and well-being? What are the research implications embedded in future epigenetic study?
What new genome sequencing technique are you most excited about and how do you think it can be applied to a question regarding aging?
How does diet and exercise change gene expression to enhance longevity?
How can genetics research help us with heredity related as well as age related hearing loss?
Genomic instability is a hallmark of both aging and cancer. How can basic aging research influence cancer therapy and drug development?
Δ133p53 represses p53-inducible senescence genes and Δ133p53α, a natural p53 isoform, contributes (by activation of hTERT expression) to conditional reprogramming and long-term proliferation of primary epithelial cells in vitro. Do you think it is possible to transfer such conditional immortalization to in vivo conditions for skin or lung rejuvenation? See https://doi.org/10.1038/s41419-018-0767-7 PMC6030220
For a patient with a particular MODY gene expression accompanyied by gene-related elevated glucose which is not supposed to increase elevated glucose-related microvascular disease associated with T2DM, what impact does this elevated glucose have on neurodegenerative disease or truly other sterile-inflammation related disease? Thank you for your reply.
How do you think genetics contribute to obesity?
Is Dr. Bredesen’s program, as described in his “End Of Alzheimer’s” book, produce permanent, reversal changes, or does it just slow the onset?