Advancing Research
by funding Grant Programs and Fellowships
Driving Innovation
by guiding studies such as the FAST Initiative, the SuperAgers Initiative, and the TAME Trial
Furthering the Field
by supporting the infrastructure of three NIA Initiatives and leading the Amplifying Geroscience Initiative.
Top Breakthroughs driven by AFAR Experts
Delaying Disease by Targeting Aging
Saving Costs by Extending Healthspan
What are the Hallmarks of Aging?
How and Why Do We Age?
What is Geroscience?
What is the Longevity Dividend?
What's Next in aging research?
Telomeres, found at the ends of our chromosomes, contain long stretches of repetitive DNA sequences that become progressively shorter with age. This has been linked to the fact that every time a cell divides, it cannot replicate the very end of our DNA molecules. So, when a cell reaches a critical telomere length, it becomes unable to divide and may die. Telomere shortening is correlated with loss of tissue function, and has been associated with degenerative aging in humans.
Dr. Batista has been studying the consequences of such telomere loss in cells. His preliminary data shows that telomere loss alters the functioning of mitochondria—organelles responsible for energy production—in pluripotent stem cells (stem cells that are capable of differentiating into many other cell types). Importantly, mitochondrial decline is a hallmark of human aging, being associated with several age-related diseases. Dr. Batista and his team hypothesize that cellular failure in aged tissues might be influenced by mitochondrial decline due to telomere shortening.
Dr. Batista is working to decipher the molecular regulation behind this telomere shortening-induced mitochondrial decline, as well as its consequences for human stem cell function. His findings will significantly increase the current knowledge on the mechanisms leading to tissue dysfunction in the elderly.
