Departments & Divisions
Institutes and Centers
Currently seeking M.S. & Ph.D. students.
Sam & Ann Barshop Institute for Longevity and Aging Studies
My lab's overarching interest is focused on delineating the fundamental mechanisms of the biology of aging to develop strategies to delay the aging process including the functional declines that lead to age-related disease, frailty and death. Aging is a biological process and interventions that slow or delay aging have the benefit of also preventing, or reversing, age-related diseases and pathology like cancer, neurodegeneration, diabetes and others. The lab's long-term goal is to translate transformative geroscience approaches discovered in basic biology towards clinical application to improve the health of aging populations.
Interventions to improve longevity and healthspan. The lab uses genetic, pharmaceutical and dietary interventions in mammalian models to better understand how longevity can be modulated and identify potential ways to move towards clinical translation. The lab is interested in better understanding how inhibition of mTOR (mechanistic target of rapamycin) is capable of extending mammalian lifespan. The mTOR signaling pathway has been shown to have a central regulatory role in aging and age-related disease through genetic or pharmaceutical (rapamycin) intervention. We are interested in expanding these findings to better understand the interplay between diet and drug interventions. In addition, we use pre-clinical non-human primate models to test the effects of rapamycin on longevity in species closely related to humans. A second significant interest is in understanding how dietary factors modulate mitochondrial function and oxidative stress during the aging process as a means to better understand pro-longevity diet interventions.
Resilience in aging. How the body responds to challenging stimuli is likely directly related to resistance to disease, pathology and potential aging. Defining such "resilience" could then have significant impact on understanding the complex phenotypes of aging. We use a novel cell-based resilience model as a potential predictive marker of aging (longevity and disease) in mammalian models. We envision the development of cellular resilience models as beneficial for personalized medicine targeted to aging and age-related disease.
Novel models of aging. Evolution has generated a world of aging models with the difference between the shortest- and longest-lived mammalian species being an order of magnitude. Probing the biology dictating such differences will help us better understand how aging is regulated. Moreover, continued development and refinement of animal and cell models has the potential to better replicate particular phenotypes of human aging.
Techniques: Animal and cellular physiology, mitochondrial and organismal metabolism
Fellow, American Aging Association
American Federation of Aging Research New Investigator in Aging Award
I01 BX004167-01A2, (Salmon), 10/01/2020-09/30/2024, Department of Veteran's Affairs,
"mTOR-Mediated Desaturation of Fatty Acids in Hepatic Insulin Resistance"
The goal of this project is to determine the interaction and effect of mTOR on lipid metabolism and its effects on insulin resistance in the liver.
U34-AG068482 (MPI: Ross and Salmon), 09/15/2020-05/31/2023, NIA
“Characterization of marmosets as a geroscience model by the San Antonio MAP”.
The goal of this project is to facilitate the characterization of the marmoset as a laboratory animal for research on aging and age-related diseases by leveraging the expertise and resources of the San Antonio Marmoset Aging Program (SA MAP).
P30 AG013319 (MPI: Strong, Hornsby, Salmon), 09/1/2020-08/31/2025, NIA
"Nathan Shock Center of Excellence in Basic Biology of Aging"
The Shock Center provides Cores to support NIA funded research grants at UTHCSA. The Aging Animal and Longevity Assessment Core breeds and “ages” thousands of mice, rats and non-human primates each year and provides investigators with lifespan data and measurements of age-sensitive traits, including body composition, food consumption, and blood collection for hormone measurement.
P30 AG044271 (MPI: Musi, Espinoza), 09/1/2020-08/31/2025, NIA
San Antonio Claude D. Pepper Older Americans Independence Center – Pre-Clinical Core
The overall objective of the San Antonio OAIC is to advance aging- and metabolism-related discoveries obtained in rodents into the pre-clinical arena using non-human primates, and from the pre-clinical arena into humans through clinical studies.
1R21AGAG067164-01 (MPI; Kamat and Salmon), 04/21/2020-03/31-2022, NIA
"Feasibility of a novel nonhuman primate model of age-related nonalcoholic fatty liver disease"
The goal of this proposal is to test the extent to which aging drives fatty liver diseases in the marmoset and the extent to which inhibition of mTOR with rapamycin may slow this progression
1R01AG057431 (PI; Salmon), 10/1/2017-9/30/2022, NIA
"Primary fibroblast resiliency as a predictor of health and lifespan in mice"
The goal of this proposal is to standardize tests of cellular resiliency using a skin-derived fibroblast model as a means to delineate the relationship between resiliency and mechanisms that regulate the aging process.
1R01 AG050797 (PI; Salmon), 09/30/2015- 06/30/2021, NIA
"The Role of mTOR Inhibition On Longevity And Healthy Aging In A Non-Human Primate"
Inhibition of the mTOR signaling pathway has been shown to extend both lifespan and healthspan in mice, but the implications of these findings for improving normal, healthy aging in humans is largely unknown. To bridge this knowledge gap, we propose testing whether mTOR inhibition by means of chronic administration of rapamycin delays aging in a non-human primate, the common marmoset, as an important step towards translational approaches to delay age-related disease in humans.
1U01AG022307 (PI; Strong), 08/15/2014 – 04/30/2024, NIA
"Center for Testing Potential Anti-Aging Interventions (NIA-Aging Interventions Testing Center)"
This is one of three national centers funded by the National Institute on Aging whose purpose is to test interventions for which therapeutic targets have been identified that have been shown to modulate the aging process.
Chair, Admissions Committee, Personalized Molecular Medicine Program. https://www.uthscsa.edu/academics/biomedical-sciences/programs/personali...
Curriculum Committee, Integrated Biomedical Science (IBMS) Graduate Program. https://www.uthscsa.edu/academics/biomedical-sciences/programs/integrated
Council of Principal Investigators, http://uthscsa.edu/artt/cpi/index.asp
Co-Director and Core-Leader, San Antonio Nathan Shock Center for Excellence in the Biology of Aging https://nathanshock.barshop.uthscsa.edu/
Core-Leader, Pre-Clinical Research Core, San Antonio Claude D. Pepper Older Americans Independence Center. https://sapepper.barshop.uthscsa.edu/pcrc/
Deputy Site Director, Interventions Testing Program (NIA). https://www.nia.nih.gov/research/dab/interventions-testing-program-itp
Board of Directors, American Aging Association. https://www.americanagingassociation.org/
Lamming DW, Salmon AB. TORwards a victory over aging. J Gerontol A Biol Sci Med Sci. 75(1):1-3. (2020) https://pubmed.ncbi.nlm.nih.gov/31544928/
Sills AM, Artavia JM, DeRosa BN, Ross CN, Salmon AB. Long-term treatment with the mTOR inhibitor rapamycin has minor effect on clinical laboratory markers in middle-aged marmosets. Am J Primatol 81(2):e22927. (2019) https://pubmed.ncbi.nlm.nih.gov/30311681/
Weiss R, Fernandez E, Liu Y, Strong R, Salmon AB, Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice. Aging (Albany, NY) 10(3):386-401. (2018) https://pubmed.ncbi.nlm.nih.gov/29579736/
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) https://pubmed.ncbi.nlm.nih.gov/25324470/
Lamming DW, Ye L, Katajisto P, Goncalves MD, Saitoh M, Stevens D, Davis JA, Salmon AB, Richardson A, Ahima RS, Guertin DA, Sabatini DM, Baur JA. Depletion of mTOR and mLST8 uncouples longevity from rapamycin-induced changes in glucose homeostasis. Science 335(6067):1638-1643. (2012) https://pubmed.ncbi.nlm.nih.gov/22461615/
Salmon AB, Kim G, Liu C, Wren JD, Georgescu C, Richardson A, Levine RL, Effects of transgenic methionine sulfoxide reductase A (MsrA) expression on lifespan and age-dependent changes in metabolic function in mice. Redox Biol 10:251-256. (2016) https://pubmed.ncbi.nlm.nih.gov/27821326/
Salmon AB. Beyond diabetes: does obesity-induced oxidative stress drive the aging process? Antioxidants (Basel) 5(3): E24. (2016) https://pubmed.ncbi.nlm.nih.gov/27438860/
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 6:401-408. (2015) https://pubmed.ncbi.nlm.nih.gov/26355396/
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) https://pubmed.ncbi.nlm.nih.gov/25558793/
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) https://pubmed.ncbi.nlm.nih.gov/23089224/
Strong R, Miller RA, Bogue M, Fernandez E, Javors MA, Libert S, Martinez PA, Murphy MP, Musi N, Nelson JF, Petrashec M, Refsnyder P, Richardson A, Salmon AB, Macchiarini F, Harrison DE. Rapamycin-mediated mouse lifespan extension: late-life dosage regimes with sex-specific effects. Aging Cell 19(11):e13269. (2020) https://pubmed.ncbi.nlm.nih.gov/33145977/
Miller RA, Harrison DE, Allison DB, Bogue M, Debarba L, Diaz V, Fernandez E, Galecki A, Garvey WT, Jayarathne H, Kumar N, Javors MA, Ladiges WC, Macchiarini F, Nelson J, Reifsnyder P, Rosenthal NA, Sadagurski M, Salmon AB, Smith Jr. DL, Snyder JM, Lombard DB, Strong R. Canagliflozin Extends Lifespan in Genetically Heterogeneous Male But Not Female Mice. JCI Insight 5(21):e140019. (2020) https://pubmed.ncbi.nlm.nih.gov/32990681/
Strong R, Miller RA, Antebi A, Astle CM, Bogue M, Denzel M, Fernandez E, Flurkey K, Hamilton KL, Lamming DW, Javors MA, de Magalhães JP, McCord JM, Miller BF, Müller M, Nelson JF, Ndukum J, Rainger GE, Richardson A, Sabatini DM, Salmon AB, Simpkins JW, Nadon NL, Harrison DE. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an α-glucosidase inhibitor or a Nrf2-inducer. Aging Cell 15(5):872-884. (2016) https://pubmed.ncbi.nlm.nih.gov/27312235/
Dorigatti AO, Hussong SA, Hernandez SF, Sills AM, Salmon AB, Galvan V. Primary neuron and astrocyte cultures from postnatal Callithrix jacchus: A non-human primate in vitro model for research in neuroscience, nervous system aging, and neurological diseases of aging. Geroscience (2021) https://pubmed.ncbi.nlm.nih.gov/33063253/
Fernandez E, Ross C, Javors M, Tardif S, Salmon AB, Evaluation of the pharmacokinetics of metformin and acarbose in a the common marmoset. Pathobiol Aging Age Relat Dis. 9(1):1657756. (2019) https://pubmed.ncbi.nlm.nih.gov/31497263/
Salmon AB, Dorigatti J, Huber H, Nathanielsz PW. Maternal nutrient restriction in baboons programs later life cellular growth and respiration of cultured skin fibroblasts: a potential model for the study of aging programming interactions. Geroscience. 40(3): 269-278, (2018) https://pubmed.ncbi.nlm.nih.gov/29802507/
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) https://pubmed.ncbi.nlm.nih.gov/19244163/
Salmon AB, Sadighi Akha AA, Buffenstein R, Miller RA. Fibroblasts from naked mole-rats are resistant to multiple forms of cell injury, but sensitive to peroxide, ultraviolet light, and endoplasmic reticulum stress. J Gerontol A Biol Sci Med Sci. 63(3):232-41. (2008) https://pubmed.ncbi.nlm.nih.gov/18375872/