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Investments in aging research will be globally transformative, providing benefits to humanity ranging from health to economics.
— Thomas Rando, M.D., Ph.D.

Thomas Rando, MD, PhD

Professor of Neurology and Neurological Sciences, Deputy Director, Stanford Center on Longevity

Thomas Rando is Professor of Neurology and Neurological Sciences at Stanford where he is the Director of the Glenn Laboratories for the Biology of Aging. He is also Chief of Neurology and Director of the Rehabilitation Research & Development Center of Excellence at the Veterans Affairs Palo Alto Health Care System. He is a founding director of the Muscular Dystrophy Association clinic at the Stanford Medical Center. Research in the Rando laboratory  focuses on tissue-specific stem cells in aging and disease, and on pathogenetic mechanisms and gene therapy for muscular dystrophies. His research on aging has demonstrated that it is possible to identify biochemical stimuli that can induce stem cells in old tissues to repair injuries as effectively as in young tissues, and this work has broad implications for the fields of regenerative medicine and stem cell transplantation.

He is a member of several professional societies, including the American Neurological Association. He is a former Paul Beeson Physician Faculty Scholar in Aging awarded by the American Federation for Aging Research and a former Ellison Medical Foundation Senior Scholar in Aging. In 2005, he received an NIH Director’s Pioneer Award for his groundbreaking research in stem cell biology. He received a BA from Harvard College, MD from Harvard Medical School and PhD in Cell and Developmental Biology from Harvard University.


FOCUS AREAS

  • Muscle Stem Cell Biology. Main areas of interest of the laboratory are muscle stem cell biology (myogenic lineage progression, cell fate determination, asymmetric cell divisions, Notch signaling, Wnt signaling)

  • Muscle Stem Cell Aging. (epigenetic determinants, local and systemic influences, roles in age-related decline in regeneration and age-related atrophy)

  • Muscular Dystrophies. (disease pathogenesis, biomarkers and non-invasive imaging), tissue engineering (artificial scaffolds, regenerative therapies)

  • Basic Muscle Cell Biology (myogenic differentiation, muscle development)

aging critical publications

  • Mueller AA, van Velthoven CT, Fukumoto K, Cheung TH, Rando TA (2016) Intronic polyadenylation of PDGFRα in resident stem cells attenuates muscle fibrosis. Nature, 540: 276-279

  • van Velthoven CTJ, de Morree A, Egner IM, Brett JO, Rando TA (2017) Transcriptional profiling of quiescent muscle stem cells in vivo. Cell Reports, 21: 1994-2004

  • Haller S, Kapuria S, Riley RR, O'Leary MN, Schreiber KH, Andersen JK, Melov S, Que J, Rando TA, Rock J, Kennedy BK, Rodgers JT, Jasper H (2017) Age-related somatic stem cell loss is a consequence of transient mTORC1 activation during regenerative episodes. Cell Stem Cell, 21: 806-818

  • Leeman DS, Hebestreit K, Ruetz T, Webb AE, McKay A, Pollina EA, Dulken BW, Zhao X, Yeo R, Ho TT, Mahmoudi S, Devarajan K, Passegue E, Rando TA, Frydman J, Brunet A (2018) Modulating the lysosome impacts protein aggregation in quiescent neural stem cells and ameliorates their ability to activate during aging. Science, 359: 1277-1283

  • Liu L, Charville GW, Cheung TH, Yoo B, Santos PJ, Schroeder M, Rando TA (2018) Impaired Notch signaling leads to a decrease in p53 activity and mitotic catastrophe in aged muscle stem cells. Cell Stem Cell, 23: 544–556