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Fri March 28, 2014
Adding Life To Your Years...
Dr. Molina will be speaking about Bioenergetics and Healthy Aging at the next Science Cafe, hosted by the River Ridge Taphouse in Clemmons. This free event is on April 8th and is sponsored by SciWorks and Reynolda Gardens. Click here for more details.
The fountain of youth has been an unattainable part of the human ethos for a long, long time. Who wouldn’t want to stay young forever? That may never be a reality, but something like it may.
The work we do at the Sticht center of aging isn’t really about extending life-span, but extending something that people have been calling health-span. We’re adding life to years instead of adding years to life.
That’s Dr. Anthony Molina, Assistant Professor of Gerontology and Geriatric Medicine at the Wake Forest Sticht Center on Aging.
There's this bioenergetic decline that happens with age. Bioenergetics is a field of study that deals with the generation and utilization of energy by living things. As we get older we feel this energy decline, and it turns out that this bioenergetic decline doesn’t just have to do with how we feel on a day to day basis but is actually involved in a lot of age-related disorders and age-related diseases. What’s not clear yet is the exact mechanisms by which this bioenergetic decline occurs.
That’s where Dr. Molina’s research comes in. His team is looking at the genetics of mitochondria. You remember, from biology class, right? If not, here’s a refresher:
Using oxygen to convert simple sugar molecules into usable energy, mitochondria are organelles, and the powerhouses of eukaryotic cells. Eukaryotic cells are cells with a nucleus, and they make up all plants and animals. Since you are made from these cells, you are essentially powered by mitochondria.
A lot of people have been focusing in on mitochondria and aging because of precisely this role of mitochondria and energy generation. What’s been known for a long time is that mitochondrial function declines over time with increasing age.
Mitochondria have been implicated in frailty, neurodegeneration (Alzheimer’s, Parkinson’s), cardiovascular disease, Type 2 Diabetes, cancer, among numerous other age-related diseases. This highlights just how fundamental this organelle is to human health. But why?
Mitochondria have their own DNA. They used to be bacteria that were free living, billions of years ago.
It is believed that mitochondria were once free-living bacterial organisms. As they evolved, they formed a symbiotic relationship with larger cells, eventually becoming dependent on living inside them, and resulting in present day eukaryotic cells.
Mitochondrial DNA harbors more mutations and deletions over time, and this is thought to contribute to the decline in their function. So there’s this genetic decline. There’re lots of things happening with increasing age that overall affect the ability of these cells to generate the “chemical currency” that cells can actually use in order to power their function.
So what are Dr. Molina and his team trying to determine in studying genetic mitochondrial decline?
What we’d like to add is measurable data that can inform physicians and healthcare providers on the best course of action for a particular patient based on their bioenergetic capacity. We’re in the very early stages of figuring out what we can measure and how we can measure it.
At the Sticht Center of Aging we always have lots of different clinical trials going on, and a lot the ones we have going on right now include testing different interventions that can potentially promote mitochondrial capacity. We just finished a trial recently, looking at caloric restriction and strength training. There’ll be future studies focused on specific nutrients or vitamins.
And though he is not yet at liberty to discuss the results,
I think generally what we can say is there are clinically amenable ways of measuring mitochondrial function, and I think that’s our biggest contribution as this point. And from here on, then we can figure out exactly what interventions could be more beneficial.