Aug 14, 2020
Professor Aditi Uday Gurkar asks
why the
aging process produces such disparate results under the same
chronology for different people.
Her research investigates
- How DNA damage reprograms a cell's metabolism and is it possible to intervene,
- How post-mitotic cells respond to DNA damage, and
- What might a unique molecular fingerprint look like for biological age based on markers, metabolites, and the metabolome.
Aditi Uday Gurkar is a principal
investigator and an assistant professor of medicine in the Division
of Geriatric Medicine at the University of Pittsburgh. Growing up
with her grandparents gave her an early view of the
aging process, but the difference between each grandparent's
health and strength struck her most of all.
This question of why people age so differently drives her research.
She explains the causes of DNA damage and mechanisms of DNA
repairing, and adds that her lab's focus is on how cells respond to
the damage. They believe they've found those responses are integral
to different levels of health as one ages.
It's estimated that one cell
will undergo 70,000 lesions or damage on any particular day. She
explains to listeners that there are many causes of DNA damage,
such as sun exposure and resulting UV radiation. The DNA repairing
signals kick in after the polymerase finds a lesion too big for its
pocket as it reads the DNA during copying and drops off. She
explains the different types of repairs in detail and that an
over-activation of repairs can lead to a cell responding as if it
is in constant stress, which drives aging.
The goal of her research is to understand how to intervene and
modulate how the cell responds, especially in reference to its
metabolism. She describes how their work with model organisms has
shown promise with such modulations and also tells listeners about
other studies, future goals, and next steps.
For more, follow her
on twitter with @healthspan_AUG and see her lab's website: agresearchlab.com.
Available on Apple Podcasts: apple.co/2Os0myK