Arlan Richardson
Studies how rapamycin slows ageing in mice, including the broad changes it causes in the liver, and co-authored early studies showing that rapamycin protects memory in Alzheimer's-model mice
Reynolds Chair in Aging Research, University of Oklahoma Health Sciences Center · Director, Oklahoma Nathan Shock Center of Excellence in the Basic Biology of Aging (2015–2022) · PhD, Oklahoma State University
Faculty profile, OU Health (Oklahoma City, Oklahoma, USA) ↗
Portrait: University of Oklahoma Health Sciences Center
Arlan Richardson has spent five decades studying the biology of aging, from the free-radical theory of aging to dietary restriction, moving through Illinois State University, the Barshop Institute at UT Health San Antonio (which he directed), and now the University of Oklahoma Health Sciences Center.
Richardson's group helped characterize how rapamycin changes the liver transcriptome and other downstream biology in treated mice, and, as a co-author of studies led by Veronica Galvan's and Salvatore Oddo's groups, helped extend the question of mTOR's role in aging into models of Alzheimer's disease, showing that rapamycin can reduce amyloid-beta levels and prevent cognitive deficits in mouse models.
The timeline below follows Richardson's contributions gathered in this Atlas.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2010 | A | Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments. CAC2010 Co-author of the 3xTg-AD mouse study showing that amyloid-beta raises mTOR signalling and that rapamycin restores memory and lowers amyloid-beta and tau, with autophagy required for the amyloid reduction. |
| 2010 | A | Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease SPI2010 Shows rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease. |
| 2012 | A | Lifelong rapamycin administration ameliorates age-dependent cognitive deficits by reducing IL-1β and enhancing NMDA signaling MAJ2012 Co-author of the study showing that rapamycin fed from 2 months of age, but not from 15 months, protected spatial memory in normally ageing mice, alongside lower brain IL-1beta. |
| 2012 | A | Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice. HAL2012 Asked whether the lifespan-extending dose of rapamycin harms or helps the aging BRAIN. Reassuringly, it enhanced learning and memory in young mice, prevented age-related cognitive decline in old ones, and even reduced anxiety and depression-like behavior - linked to boosted brain monoamines. Cognitive benefit, not cost. |
| 2012 | A | Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity LAM2012 Chronic rapamycin (about 2 mg/kg a day, close to the lifespan-extending dose) made mice glucose intolerant and insulin resistant. A clamp test placed the problem in the liver, which kept making glucose, while muscle and fat took up glucose normally. Removing mTORC1 from the liver did not cause this. Rapamycin did break up mTORC2 (it separated mTOR from Rictor) in liver, fat and muscle, and deleting Rictor in the liver alone reproduced the glucose problem. In the genetic part, female mice with one working copy each of mTOR and mLST8 had about 50% less mTORC1 signalling in the liver, normal mTORC2 signalling and normal glucose tolerance, and lived 14.4% longer on average (p = 0.046). Males did not. Boundary: mouse drug and genetics work, not people, and the lifespan gain is female-only. It supports separating the two effects, but the paper does not test a drug that blocks mTORC1 without touching mTORC2. |
| 2014 | A | Mice fed rapamycin have an increase in lifespan associated with major changes in the liver transcriptome FOK2014 Shows mice fed rapamycin have an extended lifespan associated with major changes in the liver transcriptome. |
| 2015 | A | Health Effects of Long-Term Rapamycin Treatment: The Impact on Mouse Health of Enteric Rapamycin Treatment from Four Months of Age throughout Life FIS2015 Co-author of the lifelong rapamycin health study in C57BL/6J mice, which found mixed and strongly sex-specific effects on healthspan measures rather than improvement across the board. |
Co-authors in the Atlas 19
People with a profile here who share at least one study with Arlan Richardson.
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- Randy Strong 4 shared studies Leads the San Antonio site of the NIA Interventions Testing Program, which tests each compound in parallel at three sites under one shared protocol. He first-authored the program's reports on resveratrol and other supplements (2012) and on rapamycin combined with acarbose (2022)
- Adam B. Salmon 2 shared studies Biologist of aging at UT Health San Antonio whose work in this Atlas spans rapamycin in mice and in common marmosets. He is a co-author on the Interventions Testing Program reports from the San Antonio site and on the marmoset rapamycin studies on blood markers, epigenetic age and the salivary gland
- Natalia Podlutskaya 2 shared studies Contributed, at the Barshop Institute in San Antonio, to mouse studies showing that rapamycin prevents Alzheimer's-like memory loss and improves cognition in normal ageing
- Salvatore Oddo 2 shared studies Alzheimer's disease researcher who showed that amyloid-beta raises mTOR activity and that lowering mTOR with rapamycin cuts amyloid and Tau pathology in mice through autophagy
- Veronica Galvan 2 shared studies Led mouse studies showing that rapamycin prevents Alzheimer's-like memory loss and amyloid build-up, and improves learning in normally ageing mice
- Antonella Caccamo Neuroscientist who, with Salvatore Oddo, showed in Alzheimer's model mice that amyloid-beta and mTOR feed each other in a loop that rapamycin can break
- David A. Guertin Built the mouse genetics that defined mTORC2's biological roles
- David M. Sabatini Identified mTOR (as RAFT1) in 1994. His lab then mapped much of the machinery around it: raptor and rictor at the core of mTORC1 and mTORC2, the Rag–Ragulator system that docks mTORC1 on the lysosome, and the sensors that detect leucine, arginine and SAM
- Dudley W. Lamming Showed as a postdoc that rapamycin's harm to glucose metabolism comes largely from its effect on mTORC2, while the lifespan benefit tracks mTORC1. His Wisconsin lab studies intermittent rapamycin dosing and how restricting dietary protein or single amino acids affects metabolism and ageing
- Jayanta Debnath Physician-scientist who studies how autophagy - the cell's self-digestion system - keeps epithelial tissue healthy and how tumours hijack it
- Jonathan J. Halloran First author of a 2012 mouse study showing that lifelong rapamycin does not cost the brain anything and even protects learning and memory with age; long-time member of Veronica Galvan's aging and Alzheimer's research group in San Antonio
- Joseph A. Baur Biologist of aging at the University of Pennsylvania whose lab showed that rapamycin's harm to glucose control comes from mTORC2 loss and studies how NAD levels shape health
- Kathleen E. Fischer Comparative biologist of ageing who studies why ageing rates differ between sexes, strains and species, and who led a long-term study of how lifelong rapamycin affects health measures in mice
- Patricia Spilman Neuroscientist who showed, with Veronica Galvan, that long-term rapamycin prevents memory loss in an Alzheimer's mouse model, and who later worked with Dale Bredesen on Alzheimer's drug discovery
- Smita Majumder First author of a mouse study in Salvatore Oddo's group showing that rapamycin started early in life, but not in middle age, protected against age-related memory decline
- Stacy A. Hussong Studies how mTOR damages the brain's blood vessels, and how blocking it restores blood flow, the blood-brain barrier and memory in aging and Alzheimer's models
- Steven N. Austad Comparative biologist of ageing who studies why some species and one sex live longer than others, and who directs the UAB Nathan Shock Center; senior author of a study of how lifelong rapamycin affects health in mice
- Vivian Diaz Aging researcher at the Barshop Institute in San Antonio who has worked for more than a decade on the mouse lifespan studies behind rapamycin's reputation as an anti-aging drug, including the Interventions Testing Program
- Wilson C. Fok Biologist of aging who, in Viviana Pérez's group in San Antonio, compared rapamycin with dietary restriction in mouse liver and showed that rapamycin's lifespan gain comes with large changes in liver gene activity
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