Laura Niedernhofer
Albert Einstein College of Medicine, NY·Genetics
Some people reach 100 in good health, and a handful of rare changes in their DNA appear to be part of the reason. If those changes can be shown to actually cause better health in old age, the genes and pathways they affect become candidate targets for drugs that extend the healthy portion of life rather than just lifespan.
- Fields
Genetics
Biochemistry
Pharmacology
- Topics
aging
healthspan
longevity
- Grants
- 1 known grant, through Aug 2028
What they work on
- Test whether rare gene variants found in centenarians extend healthspan by installing the mutation, or raising or lowering gene activity, in Ercc1-deficient mice, which have faulty DNA repair and age about six times faster than normal mice.
- Characterize mice already generated to carry specific longevity variants, including the centenarian IGF1R variant and mice with one working copy of Smad3, Foxo3a or Usp35, measuring health, resilience and age-related tissue damage.
- Separate which of SIRT6's two enzyme activities matters for healthy aging, using mice with mutations that remove either its deacetylase function or its ADP-ribosyltransferase function.
- Determine whether pharmacologically blocking the same pathways improves aging outcomes, testing compounds such as the IKK/NF-kB inhibitor SR12343 and the ATM inhibitor KU-55933 in fast-aging and naturally aged mice.
- Quantify cellular senescence, the state where damaged cells stop dividing and emit inflammatory signals, and other molecular hallmarks of aging as readouts for each genetic and drug intervention in mouse tissues.
More about the research
This project's job within a larger multi-project program is the test step: taking variants found in people and checking, in mice, whether altering the same gene or pathway really improves health with age.
Why it matters
Age is the dominant risk factor for most chronic disease, so interventions that delay aging itself could reduce many conditions at once. By checking in mice whether rare gene variants carried by exceptionally healthy centenarians genuinely improve health with age, and whether drugs aimed at the same pathways do the same, this work could confirm which of these targets are worth pursuing for therapies that extend healthy years of life.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xiaohong Lu
Louisiana State University Health Sciences Center-Shreveport, LA·Neuroscience
Determine whether SARS-CoV-2 infection drives chronic loss of smell and cognitive deficits in humanized ACE2 transgenic mice, in a model that produces lasting brain pathology without the virus invading the brain.
Christian Sell
Drexel University, PA·Biology
Test whether rapamycin, a drug that blocks the mTOR growth pathway, prevents cellular senescence (permanent cell-cycle arrest) by raising levels of the long non-coding RNA H19.
Jenna Bartley
University of Connecticut, CT·Microbiology & Immunology
Test whether clearing senescent cells with senolytic drugs before vaccination improves cell-mediated and antibody responses to recombinant flu nucleoprotein and adjuvanted inactivated flu vaccines in aged mice.
The school
Albert Einstein College of Medicine: 21 labs on PI Pages, $361M a year on research, 36 research doctorates a year.
Reach out
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