Brian K. Kennedy
Co-discovered that inhibiting the TOR pathway is the single strongest lifespan-extending intervention in a genome-wide yeast deletion screen
PhD, MIT (Leonard Guarente lab) · postdoc, Massachusetts General Hospital Cancer Center · Assistant/Associate Professor, University of Washington (with Matt Kaeberlein) · President & CEO, Buck Institute for Research on Aging (2010–2016) · now Distinguished Professor of Biochemistry & Physiology, National University of Singapore (since 2017)
Faculty profile, National University of Singapore ↗
In 2005, Kennedy and Matt Kaeberlein, working together at the University of Washington, systematically deleted 564 individual genes in yeast and measured how long each mutant strain lived. The strongest lifespan-extending hits, by a wide margin, were genes in the TOR (Target Of Rapamycin) and Sch9 pathway — the first genome-scale evidence, rather than a single-gene hunch, that dialing down nutrient-sensing signaling through TOR is one of the most powerful levers for extending lifespan, in an organism as simple as budding yeast.
Kennedy trained with Leonard Guarente at MIT, whose lab had linked sirtuins to yeast aging, then moved into aging research proper as a UW faculty member working alongside Kaeberlein. In 2010 he took over as President and CEO of the Buck Institute for Research on Aging, where he spent six years building it into one of the field's leading independent aging-research institutes.
Since 2017 Kennedy has been Distinguished Professor of Biochemistry and Physiology at the National University of Singapore, where he directs the Healthy Longevity Translational Research Programme — work focused on translating basic geroscience, including TOR biology, into biomarkers and interventions that could delay human aging rather than just treat individual age-related diseases.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2005 | A | Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients KAE2005 A systematic screen of 564 yeast gene deletions identifies TOR and Sch9 pathway genes as the single strongest lifespan-extending hits, establishing nutrient-sensing signaling as a central, targetable axis of aging. |
| 2016 | R | The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging KEN2016 A review argues mTOR acts as the coordinating hub of whole-body metabolism and lays out why mTORC2 inhibition underlies rapamycin's metabolic side effects — the main obstacle to repurposing it as an anti-aging drug. |
On the programme
Meetings in the Atlas calendar where Brian K. Kennedy is listed among the speakers or organisers.
- upcoming Keystone Symposia: Healthy Aging & Therapeutic Opportunities 2027 ↗ 12–15 Apr 2027 · Taipei, Taiwan · Tier 2