- Understanding the basic biology of aging by using targeted interventions to delay the aging process in mammals. A focus on the lab is understanding how the inhibition of the mTOR signaling pathway can be used to delay aging and improve health. We use both rodents and non-human primates as model systems to address these questions. Some key questions we address are 1) does mTOR inhibition have similar effects in both model systems, 2) can diet interact with the pro-longevity effects of mTOR inhibition, 3) could multi-drug treatments be used to promote longevity and reduce potential side-effects.
- Determining whether modulation of oxidative stress could regulate healthy lifespan; i.e., does reduction of oxidative stress slow the development of age-related disease? In particular, we are interested in studying the role of oxidative stress and protein oxidation in the development of metabolic dysfunction with age and obesity. The oxidative stress theory of aging has been one of the most prominent theories of why organisms age. Both aging and increased fat accumulation promote dysregulation of glucose metabolism, alterations in adipose tissue homeostasis, and declines in cellular function that are detrimental to overall health. Metabolic diseases like Type 2 diabetes currently affect a significant proportion of the world's population and their prevention could certainly lead to longer, healthier lives.
Liu R, Pulliam DA, Liu Y, Salmon AB, Dynamic differences in oxidative stress and the regulation of metabolism with age in visceral versus subcutaneous adipose. Redox Biol. (2015). in press.
Salmon AB, Lerner C, Ikeno Y, Motch Perrine S, McCarter R, Sell C. Altered metabolism and resistance to obesity in long-lived mice producing reduced levels of IGF-1. Am J Physiol Endo Metabol 308(7):E545-E553. (2015). PMCID: PMC4385875.
Zhang Y, Fischer KE, Soto V, Liu Y, Sosnowska D, Richardson A, Salmon AB, Obesity-induced oxidative stress, accelerated functional decline with age and increased mortality in mice. Arch Biochem Biophys 576:39-48. (2015). PMCID: PMC4456198.
Liu Y, Diaz V, Fernandez E, Strong R, Ye L, Baur JA, Lamming DA, Richardson A, Salmon AB. Rapamycin-induced metabolic defects are reversible in both lean and obese mice. Aging (Albany, NY) 6(9):742-754. (2014). PMCID: PMC4221917.
Tardif S, Ross C, Bergman P, Fernandez E, Javors M, Salmon A, Spross J, Strong R, Richardson A. Testing efficacy of administration of the anti-aging drug rapamycin in a non-human primate, the common marmoset. J Gerontol A Biol Sci Med Sci. 70(5):577-588. (2015). PMCID: PMC4400395
Edrey YH, Salmon AB. Revisiting an age-old question regarding oxidative stress. Free Rad Biol Med 71C:368-378. (2014). PMCID: PMC4049226.
Liu Y, Qi W, Richardson A, Van Remmen H, Ikeno Y, Salmon AB. Oxidative damage associated with obesity is prevented by overexpression of CuZn- or Mn-superoxide dismutase. Biochem Biophys Res Comm 438(1):78-83. (2013). PMCID: PMC3768142.
Styskal J, Nwagwu FA, Watkins YN, Liang H, Richardson A, Musi N, Salmon AB. Methionine sulfoxide reductase A affects insulin resistance by protecting insulin receptor function. Free Rad Biol Med 56:123-32. (2013). PMCID: PMC3578155.
Salmon AB, Pérez VI, Bokov A, Jernigan A, Kim G, Zhao H, Levine RL, Richardson A. Lack of methionine sulfoxide reductase A in mice increases sensitivity to oxidative stress but does not diminish lifespan. FASEB J 23(10):3601-8. (2009). PMCID: PMC2747676.
Salmon AB, Leonard SL, Masamsetti V, Pierce A, Podlutsky AJ, Podlutskaya N, Richardson A, Austad SN, Chaudhuri AR. The long lifespan of two bat species is correlated with resistance to protein oxidation and enhanced protein homeostasis. FASEB J 23(7):2317-2326. (2009). PMCID: PMC2704589.