MedicalResearch.com Interview with:
Douglas P. Kiel, MD, MPH
Professor of Medicine
Harvard Medical School
Director Musculoskeletal Research Center
Institute for Aging Research, Hebrew SeniorLife
Associate Member Broad Institute of Harvard and MIT
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Why we age? and how we age?, are perennial questions that are of interest to all. The research described in this publication brings together two major and different concepts of aging - epigenetic aging, which is manifested by modifications on DNA and telomere-related aging, which is manifested by shortening of chromosome ends (telomeres). In our search for genes that could potentially affect epigenetic aging, we detected a variant of the
TERT gene (whose encoded protein, telomerase maintains telomere length) to be associated with accelerated epigenetic aging. TERT is a subunit of the enzyme telomerase which is a widely known enzyme for the following reasons:
1) Telomerase has been touted as an anti-aging enzyme. It has been called a modern fountain of youth. However, some scientists have pointed out that it is unlikely to become a source of anti-aging therapies (see the review article by de Magalhães JP1, Toussaint in Rejuvenation Research (2004) .
https://www.ncbi.nlm.nih.gov/pubmed/15312299) Our new results gained by the epigenetic clock also indicate that telomerase will not halt organismal aging.
2) The book "The Telomere Effect" by Nobel prize winner Elizabeth Blackburn and Elissa Epel was on the New York Times best seller list and received substantial news coverage:
https://www.cbsnews.com/news/telomere-effect-book-living-younger-healthier-longer/
Our data provides a much needed understanding of the molecular drivers of the epigenetic clock and reveal a unexpected and paradoxical connection between two seemingly distinct aging clocks: the telomere clock and the epigenetic clock.
Our main finding was that variants in the human telomerase reverse transcriptase gene (
TERT) were associated with increased “intrinsic epigenetic aging.”
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