Nearly half a million dollars is coming to San Antonio to support aging research conducted by Robert A. Marciniak, M.D., Ph.D., assistant professor of medicine and cellular and structural biology at The University of Texas Health Science Center at San Antonio.
The American Federation for Aging Research (AFAR) and the Alliance for Aging Research awarded $450,000 to Dr. Marciniak, who is studying the molecular biology of human aging. Dr. Marciniak is a 2002-2005 Paul Beeson Physician Faculty Scholar, one of the most prestigious designations in the field of aging research.
"We are extremely pleased to recognize the cutting-edge research that Dr. Marciniak is conducting on oxidative stress and telomere maintenance," said William R. Hazzard, M.D., chair of the Beeson program committee and professor at the University of Washington School of Medicine. "We are hopeful that his research will lead to a better understanding of the root causes of aging at the cellular level."
Some researchers theorize that aging occurs because normal biological processes release reactive oxygen that can damage cells. Telomeres, the structures that protect and stabilize cells by capping the ends of our chromosomes, are known to shorten in many of our cells as we get older, which can cause cells to stop dividing or die. Dr. Marciniak is investigating whether oxidative stress contributes to telomere loss in humans.
A Harvard-trained physician and molecular biologist who completed postdoctoral work at MIT, Dr. Marciniak is interested in aging especially as it relates to cancer. "There may be no more challenging area of study than aging," he said. "We're asking questions about the development of age-related pathologies, such as cancer, with the goal of understanding the underlying processes. It's still debated whether aging can be studied as a whole or whether it should be broken down by disease - cancer, cardiovascular disease, neurodegenerative disorders and so forth. But previous work done at the Health Science Center showed that diverse processes can be modulated by one simple environmental manipulation - calorie restriction - at least in mice."
He based his decision to join the Health Science Center partly on the number of faculty who define themselves by their interest in aging research. "The Health Science Center is second only to the National Institute on Aging in this field," Dr. Marciniak said. "When I was looking at universities, this became clear."
He also seeks to understand disorders such as Werner syndrome, which is characterized by accelerated aging. Individuals with Werner syndrome are healthy at birth, but their adolescent growth is diminished. By their 20s, they develop cataracts, connective tissue changes and gray hair. "We're trying to understand what the Werner syndrome protein is doing in telomeres and how this is related to accelerated aging," Dr. Marciniak said.
Hutchison-Gilford syndrome is another human genetic disorder of accelerated aging. In contrast to Werner syndrome, changes are evident at birth. Adults with Werner syndrome develop cardiovascular disease in their 20s and 30s, but children affected by Hutchinson-Gilford develop it in their teens or earlier. "These children die of cardiovascular disease that looks identical to normal cardiovascular disease," Dr. Marciniak said. "We are trying to analyze how defects in telomere maintenance and processing in these disorders may lead to these problems and relate this to the problems we all experience as we grow older."
Note: Robert A. Marciniak, M.D., Ph.D. bio