Sinclair Lab (Harvard Medical School)
Academic
About
The Sinclair Lab in the Department of Genetics at Harvard Medical School, part of the Paul F. Glenn Center for Biology of Aging Research, studies why organisms age and whether ageing can be slowed or reversed. Its early work concerned sirtuins, NAD+ metabolism and small-molecule SIRT1 activators such as resveratrol. The current programme centres on the 'information theory of aging', which holds that loss of epigenetic information drives ageing: the lab built the ICE mouse, in which induced DNA breaks accelerate epigenetic ageing, and uses viral delivery of the reprogramming factors Oct4, Sox2 and Klf4 to restore youthful gene expression, with a focus on nerve and optic regeneration. Other projects cover DNA repair, fertility, mitochondria and muscle loss. The work matters for ageing research because it tests whether epigenetic age can be reset in living tissue, an idea now being tested clinically by Life Biosciences, a company Sinclair co-founded.
Rating breakdown
Aggregate 60/100 · rank #12 in the academic & non-profit table full ratings →
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Publications80
- David Sinclair — h-index 122 source ↗
- Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan (Howitz et al., Nature, 2003) ↗
- Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging (Gomes et al., Cell, 2013) ↗
- Reprogramming to recover youthful epigenetic information and restore vision (Lu et al., Nature, 2020) ↗
- Loss of epigenetic information as a cause of mammalian aging (ICE mouse; Yang et al., Cell, 2023) ↗
- Resveratrol improves health and survival of mice on a high-calorie diet (Baur et al., Nature, 2006) ↗
Discovery39
Trials from ClinicalTrials.gov (this org as lead sponsor), matched to aging by their condition or intervention.
Fundraising88
Grants of the organisation's listed people, name-matched via NIH RePORTER ↗.
- David Sinclair: Using cellular co-biosis and age programmable mice to derive a global interaction map of aging hallmarks · USD 436K · National Institute on Aging 5R01AG082737-03
- David Sinclair: Using cellular co-biosis and age programmable mice to derive a global interaction map of aging hallmarks · USD 436K · National Institute on Aging 5R01AG082737-04
Education16
- David Sinclair public communicator
- David Sinclair ARDD speaker 2024;2026 source ↗
Key outputs
- publication Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan (Howitz et al., Nature, 2003) ↗ 2003
- publication Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging (Gomes et al., Cell, 2013) ↗ 2013
- publication Reprogramming to recover youthful epigenetic information and restore vision (Lu et al., Nature, 2020) ↗ 2020
- publication Loss of epigenetic information as a cause of mammalian aging (ICE mouse; Yang et al., Cell, 2023) ↗ 2023
- publication Resveratrol improves health and survival of mice on a high-calorie diet (Baur et al., Nature, 2006) ↗ 2006
- publication Chemically induced reprogramming to reverse cellular aging (Yang et al., Aging, 2023) ↗ 2023
- dataset or tool FRIGHT and AFRAID mouse frailty clocks: open web app and code predicting biological age and lifespan from a murine frailty index (Schultz, Kane et al., 2020) ↗ 2020
Investment & funding
| Date | Type | Amount | Detail | Counterparties |
|---|---|---|---|---|
| 2026 | grant | USD 436K | Sinclair Lab (PI David A. Sinclair) publicly disclosed (NIH RePORTER) FY2026 award for R01AG082737, 'Using cellular co-biosis and age programmable mice to derive a global interaction...' | National Institute on Aging (NIH) |
Key people
Research fields
Links
Sources
- https://sinclair.hms.harvard.edu/
- https://sinclair.hms.harvard.edu/people
- https://sinclair.hms.harvard.edu/people/david-sinclair
- https://sinclair.hms.harvard.edu/research
- https://agingresearch.hms.harvard.edu/faculty/sinclair/
- https://genetics.hms.harvard.edu/faculty-staff/david-andrew-sinclair
- https://sinclair.hms.harvard.edu/david-sinclairs-affiliations
- https://reporter.nih.gov/project-details/11370116