Ph.D. 2004, University of Chile
Postdoc 2004-2011, Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio
Currently, my laboratory is focused primarily on understanding the mechanisms by which rapamycin, an mTOR inhibitor, improves healthspan and extends longevity in mice, including Alzheimer’s disease mouse models. The target of rapamycin (TOR) is a major signaling hub that integrates nutrient/ growth factor availability with cell metabolism. Rapamycin, a TOR inhibitor, is the first drug that has been experimentally proven to slow down aging in mice. At the cellular level, it has been shown that rapamycin can inhibit cellular senescence in many cell types in vitro. Our recent work demonstrated that rapamycin decreases cellular senescence in vivo, including a reduction of proinflammatory cytokines in serum and several tissues including brain. Thus, we believe that this increase in SASP by senescent cells contributes to the precipitation of loss of function in several tissues. Thus, our primary goal is to understand the role of senescent cells and SASP in the development of age-related pathologies, including Alzheimer’s disease.
Another interest of my research group is to determine the role of proteostasis mechanisms (chaperones, autophagy, and proteasome) in aging using a comparative biology approach. Previously in our laboratory, we found that cells from long-lived species (i.e., little brown bat and naked mole rat) have a more robust proteostasis than short-lived species (i.e., naked mole rats vs. mouse), suggesting that long-lived species might have evolved enhanced proteostasis activities to preserve protein structure and prevent protein misfolding and aggregation. Thus, using a comparative biology approach, my laboratory currently is investigating if cells from long-lived species are more resistant to proteotoxicity (protein aggregation) than their short-lived counterparts.