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Ronald DePinho: Aging and Cancer Research Elucidates Neurodegenerative Mechanisms and Treatments
Manage episode 434198837 series 3558288
Το περιεχόμενο παρέχεται από το Mark Mattson. Όλο το περιεχόμενο podcast, συμπεριλαμβανομένων των επεισοδίων, των γραφικών και των περιγραφών podcast, μεταφορτώνεται και παρέχεται απευθείας από τον Mark Mattson ή τον συνεργάτη της πλατφόρμας podcast. Εάν πιστεύετε ότι κάποιος χρησιμοποιεί το έργο σας που προστατεύεται από πνευματικά δικαιώματα χωρίς την άδειά σας, μπορείτε να ακολουθήσετε τη διαδικασία που περιγράφεται εδώ https://el.player.fm/legal.
Cells in all organ systems experience the same ‘hallmarks of aging’ which include the accumulation of oxidatively damaged proteins, DNA, membranes and mitochondria, impaired DNA repair and autophagy, senescence, and inflammation. In this episode Professor Ron DePinho of the MD Anderson Cancer Center in Houston talks about his remarkable career during which he and his trainees established fundamental mechanisms that control cell proliferation and differentiation in normal development and how alterations in these mechanisms result in aging and cancers. He then describes how the telomerase protein influences hallmarks of aging by controlling gene expression, and how age-related reductions in telomerase levels contribute to normal aging and the pathogenesis of Alzheimer’s disease. Ron and his colleagues have recently identified a chemical called TAC that can increase telomerase levels in cells. Treatment of old mice with TAC rejuvenates multiple organ systems, and can restore neuroplasticity and cognition in mouse models of Alzheimer’s disease.
LINKS:
DePinho laboratory web page:
https://www.mdanderson.org/research/departments-labs-institutes/labs/depinho-laboratory.html
Related Articles:
https://www.cell.com/action/showPdf?pii=S0092-8674%2820%2931750-5
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733214/pdf/nihms487161.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8759755/pdf/nihms-1761822.pdf
https://pubmed.ncbi.nlm.nih.gov/38908367/
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