Richardson began his academic career in 1968 as an Assistant Professor in the Department of Chemistry at Fort Lewis College,a role he held until 1969. In 1971,he joined Illinois State University,where he served as an Assistant Professor in the Department of Chemistry from 1971 to 1974,an Associate Professor from 1974 to 1979,and a Professor from 1979 to 1990. Between 1986 and 1990,he also held the position of Distinguished Professor in the Board of Regents of the State of Illinois. In 1990,he joined the University of Texas Health Science Center San Antonio. There,he served as a Professor in the Department of Medicine from 1990 to 1995,a Professor in the Department of Physiology from 1995 to 2003,and a Professor in the Department of Cellular and Structural Biology from 2003 to 2013. He joined the University of Oklahoma Health Sciences Center,where he served as a Professor in the Department of Geriatric Medicine from 2013 to 2019. Since 2019,he has been a Professor in the Department of Biochemistry and Physiology at the same institution.[1]
Richardson served as President of both the Gerontological Society of America and the American Aging Association. From 1995 to 2013,he served as the Director of the San Antonio Nathan Shock Center of Excellence in Basic Biology of Aging. Since 2013,he has held the Donald W. Reynolds Endowed Chair of Aging Research at the University of Oklahoma Health Sciences Center.[1]
Research
Richardson's research has explored the biology of aging,focusing on the roles of dietary restriction,oxidative stress,mitochondrial dysfunction,genetic regulation,and epigenetic modifications in the aging process and related diseases. His initial research studied the molecular pathways responsible for the anti-aging effects of dietary restriction. His laboratory was the first to show that dietary restriction altered gene expression through changes in the activity of transcription factors.[3][4]
Richardson also examined age-associated oxidative DNA damage,showing that levels of 8-oxo-2-deoxyguanosine (oxo8dG),a marker of oxidative DNA damage,increase with age in nuclear and mitochondrial DNA across various tissues and species.[5] His research also demonstrated that dietary restriction,known to extend lifespan,mitigates this oxidative damage,providing indirect support for the oxidative stress theory of aging.[6] He studied the effect of oxidative damage/stress on aging using genetically engineered mouse models to alter the expression of antioxidant enzymes on aging. His first experiments on heterozygous manganese superoxide dismutase (MnSOD) knockout mice revealed that reduced MnSOD activity leads to increased oxidative damage,mitochondrial dysfunction,and an elevated incidence of cancer,though without accelerating aging.[7][8] Subsequent studies,using both transgenic and knockout mice,found limited evidence that oxidative stress significantly influences lifespan,although it may contribute to age-related diseases such as cancer.[9][10]
In his research on the molecular mechanisms of aging beyond oxidative stress,Richardson explored the role of the mammalian target of rapamycin (mTOR) pathway,showing that its inhibition by rapamycin extends lifespan in mice and ameliorates cognitive deficits and amyloid-beta pathology in Alzheimer's disease models.[11][12] However,he also identified that rapamycin-induced longevity is independent of insulin sensitivity,implicating distinct pathways in the regulation of aging and metabolic health.[13] In 2018,he studied the pathways responsible for chronic inflammation (inflammaging),which occurs with age. He was the first to show that the cell death pathway of necroptosis contributed to inflammaging[14] and that necroptosis induces cell senescence.[15][16]
Awards and honors
1993 –Nathan W. Shock Award,Gerontology Research Center of the National Institute on Aging
1995 –Robert W. Kleemeier Award,Gerontological Society of America[17]
2001 –Harman Research Award,American Aging Association
2008 –Irving Wright Award,American Federation for Aging Research[18]
Richardson,A.,Butler,J. A.,Rutherford,M. S.,Semsei,I.,Gu,M. Z.,Fernandes,G.,&Cheung,W. H. (1987). Effect of age and dietary restriction on the expression of α2u-globulin. Journal of Biological Chemistry,262(27),12821–12825.
Hamilton,M. L.,Van Remmen,H.,Drake,J. A.,Yang,H.,Guo,Z. M.,Kewitt,K.,... &Richardson,A. (2001). Does oxidative damage to DNA increase with age? Proceedings of the National Academy of Sciences,98(18),10469–10474.
Pérez,V. I.,Bokov,A.,Van Remmen,H.,Mele,J.,Ran,Q.,Ikeno,Y.,&Richardson,A. (2009). Is the oxidative stress theory of aging dead? Biochimica et Biophysica Acta (BBA) - General Subjects,1790(10),1005–1014.
Caccamo,A.,Majumder,S.,Richardson,A.,Strong,R.,&Oddo,S. (2010). Molecular interplay between mammalian target of rapamycin (mTOR),amyloid-β,and Tau:Effects on cognitive impairments. Journal of Biological Chemistry,285(17),13107–13120.
Richardson,A. (2013). Rapamycin,anti-aging,and avoiding the fate of Tithonus. Journal of Clinical Investigation,123(8),3204–3206.
Deepa,S. S.,Unnikrishnan,A.,Matyi,S.,Hadad,N.,&Richardson,A. (2018). Necroptosis increases with age and is reduced by dietary restriction. Aging Cell,17(2),e12770.
Sathiaseelan,R.,Ahn,B.,Logan,S.,Wanagat,J.,Nguyen,H. V. M.,Hord,N. G.,Vandiver,A. R.,Selvarani,R.,Ranjit,R.,Yarbrough,H.,Masingale,A.,Miller,B. F.,Wolf,R. F.,Stout,M. B.,Austad,S. N.,&Richardson,A. (2023). A genetically heterogeneous rat model with divergent mitochondrial genomes. The Journals of Gerontology:Series A,78(5),771–779.
↑ "Effect of age and dietary restriction on the expression of alpha 2u-globulin". PMID2442168.{{cite web}}: Missing or empty |url= (help)
↑ "Expression of heat shock protein 70 is altered by age and diet at the level of transcription". PMID7682654.{{cite web}}: Missing or empty |url= (help)
↑ "The role of oxidative damage and stress in aging". PMID15541775.{{cite web}}: Missing or empty |url= (help)
↑ "Increased oxidative damage is correlated to altered mitochondrial function in heterozygous manganese superoxide dismutase knockout mice". PMID9774481.{{cite web}}: Missing or empty |url= (help)
↑ "Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging". PMID14679299.{{cite web}}: Missing or empty |url= (help)
↑ "Is the Oxidative Stress Theory of Aging Dead?". PMC2789432.{{cite web}}: Missing or empty |url= (help)
↑ "Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease". PMID20376313.{{cite web}}: Missing or empty |url= (help)
↑ "Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments". PMID20178983.{{cite web}}: Missing or empty |url= (help)
↑ "Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity". PMID22461615.{{cite web}}: Missing or empty |url= (help)
↑ "Necroptosis increases with age and is reduced by dietary restriction". PMID29696779.{{cite web}}: Missing or empty |url= (help)
↑ "Necroptosis contributes to chronic inflammation and fibrosis in aging liver". PMID34761505.{{cite web}}: Missing or empty |url= (help)
↑ "Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma". PMID35869934.{{cite web}}: Missing or empty |url= (help)
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