Prolonging your healthy years: an interview with Aric Rogers

Written by Freya Leask

In this interview, Aric Rogers, PhD, assistant professor at the MDI Biological Laboratory (Bar Harbor, Maine, USA), discusses how factors such as genetic variations and environmental conditions influence lifespan.

The MDI Biological Laboratory (Bar Harbor, Maine, USA) is a growing, independent, biomedical research institution. It aims to improve human health and wellbeing through basic research and development ventures, as well as providing world-class science education.

In this interview, Aric Rogers, PhD, assistant professor at the MDI Biological Laboratory, discusses how he is studying factors such as genetic variations and environmental conditions that can influence lifespan using roundworms.

Aric Rogers, PhD

Aric Rogers, PhD, is an assistant professor at the MDI Biological Laboratory in Bar Harbor, Maine. He holds a doctorate from the University of Massachusetts in molecular and cellular biology and performed his postdoctoral research at the Buck Institute for Research on Aging. Using the roundworm, C. elegans, Rogers studies how gene expression is altered under conditions that extend lifespan, particularly at points of regulation occurring after transcription. In particular, he studies the genetic mechanisms underlying the life-prolonging effects of dietary restriction, which has been found to extend lifespan in a range of species. Because environment influences genes controlling aging and health, interventions like dietary restriction can delay, prevent or otherwise mitigate the severity of age-related diseases, including diabetes, cancer and neurodegeneration. The goal of his research is to understand how lifespan-extending interventions work across different species and to apply what is learned to improving healthy human lifespan.

Could you introduce yourself and give some background on the MDI Biological Laboratory?

I’m an assistant professor at the MDI Biological Laboratory, where our focus is on aging and regeneration. Our approach is to study the molecular mechanisms that underlie aging and regeneration by using animals that can teach us the most about these phenomena. Our goal is to use what we learn to improve human health by slowing the physiological decline associated aging and to stimulate regeneration of damaged tissues.

How did you come to work in the MDI Biological Laboratory?

I came with a background in the biology of aging and there are a few centers around the country that have this focus. Although the MDI Biological Laboratory has only relatively recently shifted its focus to aging, what really attracted me was that they were also focused on this issue of regeneration. I think that these two areas — trying to slow the biological processes that contribute to aging as well as to stimulate the regeneration of damaged tissues — are going to be two of the most therapeutically promising areas to prolong the healthy years of life.

What is it that interests you in age-related disease and regenerative medicine?

It’s hard not to be interested in these topics — everyone ages. Adults experience declines in tissue function and quality of life as we grow older, and an increase in our understanding of the interactions between our genes and the environment, along with new drug development or repurposing of drugs that already exist, has put us in a special position. For the first time, we actually have the potential to ameliorate the decline in health that we all experience.

Why are you using roundworms as a model for your studies, as opposed to other model organisms such as the zebrafish?

One of the things I came to appreciate as I got into the biological sciences was that nature doesn’t waste what works. Although we may look very different, the way our cells grow and communicate at the molecular level is very well preserved, even among seemingly disparate species.

The revolution in our understanding of the biological processes that influence aging really started with the small roundworm, C. elegans, in the late eighties and early nineties and this organism continues to teach us about how evolutionarily preserved genetic pathways influence health and longevity. The other useful aspect is that there are no restrictions for animal use with invertebrates such as C. elegans. The animals grow to adulthood in 3 days and they only live for 3 weeks, which makes them perfect for figuring out which genes control resilience to stress and longevity.

What are the challenges you have come across in your research?

There have been lots of challenges. The science is a challenge, as is running a lab. I’m still a new principal investigator and currently the biggest challenge to my time and effort has been developing grant applications for federal funding, which is incredibly competitive right now.

How have these been overcome, or if not, what could help this?

I’m still overcoming them! It’s basically a lot of time and effort and not giving up, of pushing forward, no matter what.

You are studying the molecular mechanisms underlying the life-prolonging effects of dietary restriction – what are the potential clinical implications of this research?

Dietary restriction can involve multiple forms of restricting and changing diet, but one of the most common ways is simply to limit calories. There are many ways that that this type of dietary intervention works to increase lifespan and it’s one of the most easily accessible ways that we have to increase health and longevity in just about every organism that has been tested. That suggests that this holds a lot of promise for us — we’re just another animal on this planet so if dietary restriction works in a worm and a fly and a mouse, it has some promise of working in us. Unfortunately, the extremity of the dietary restriction regimen can make it very difficult to follow, and there are other drawbacks as well.

The good thing is that we’re beginning to get a picture of how gene activity changes under dietary restriction and how that’s coordinated. That means we can therapeutically target proteins that control that coordinated effort to get the same or similar results without having to go to the extent of starving ourselves or putting ourselves on very difficult-to-maintain diets.

How important for age-related disease is understanding the relationship between genetic variations and environmental conditions?

It’s hugely important. It’s becoming increasingly clear that there are many environmental factors that affect the maintenance of health and aging. With respect to diet, it’s not just about the amount but the type of food. There are lots of things, including exercise, that influence the activity of our genes and a big part of what we’re trying to figure out is which gene changes are associated with promoting health.

We’re also now moving into the age of personalized medicine. Even though we all have the same genes, there are small variations that can influence gene activity. Therefore, although we have some understanding of the major genetic pathways that influence aging through single genes, we’re really only scratching the surface of how small variations in many genes simultaneously could add to or detract from how quickly we age.

What are the next steps in your research?

We recently discovered that there are certain ways of limiting protein synthesis within cells, which is something that happens as a result of dietary restriction, to increase health and resistance to age-related disease. We found that genetically attenuating protein synthesis activates a specific cellular program that helps get rid of molecular clutter. Now we are applying for a grant to figure out exactly how that works.

What’s really cool is that this intervention also increases the ability of the body to deal with malformed and misshapen proteins that tend to aggregate and that are associated with age-related diseases like Alzheimer’s and Parkinson’s. If we figure out how this works, we can test the results in other species. Ultimately, we hope that this discovery and other discoveries like this could be used to develop therapeutics to improve the health of our own tissues and prevent, or at least delay, the onset of these types of age-related disease.

Where do you see the field of regenerative medicine and age-related disease heading in the next 10 years?

The biomedical community is on the cusp right now of taking information from aging research and applying it to improve human health. The first test that is on the immediate horizon is the repurposing of a drug called metformin. It’s been around for a very long time to treat type 2 diabetes. The pathway that the drug influences to control blood sugar is one that we know to extend lifespan, from worms all the way up to mice. The study will be carried out to look at changes in all causes of morbidity in a population of seniors.

What’s interesting is that there has been a study looking at people who are on this drug that found that some of the people with diabetes that were taking metformin were actually living longer than their non-diabetic counterparts. The good thing for us in this new foray into trying to slow age-related decline is that this drug is very cheap. It could potentially be the first healthspan-extending drug in humans that will be widely available. However, this is just the first one; there are others in the queue.

This is really the beginning of a new era for us of being able to control aging and age-related health conditions and that’s very exciting. In addition to efforts to find a cure that is, say, specific for Alzheimer’s and a different one for cancer, we might also be able to take a single preventative medicine that helps protect us from many or all age-related diseases. That’s really exciting — I would say stay tuned!

Acknowledgements/Disclosure

  • Nothing to acknowledge or disclose

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