Research - February 2012 Archives

JACKSONVILLE, Fla. — Vitamin D is primarily produced in the body through direct exposure of the skin to sunlight. While it has long been touted for its important role in maintaining healthy bones, more recent research suggests that sustaining healthy levels of vitamin D in the bloodstream can also reduce the risk of common diseases such as heart disease, diabetes and some types of cancer, says a Mayo Clinic researcher. "Unfortunately, many Americans are unaware of these additional health benefits of vitamin D, and some reports suggest that up to one-quarter of the U.S. population have suboptimal levels of vitamin D in their blood — a condition known as hypovitaminosis D," says Alexander Parker, Ph.D., associate professor of epidemiology and urology at Mayo Clinic, Florida, and chair of the Division of Health Sciences Research. One segment of the U.S. population that is at particular risk of having lower than optimal vitamin D levels is the black community, he says. This is primarily because darker skin, with more melanin, reduces the ability to absorb the sunlight necessary to make vitamin D, Dr. Parker says. "Indeed, data from large, national studies have reported that as high as 40 percent of black Americans in the U.S. do not have healthy levels of vitamin D in their blood," he says. "That's important because low vitamin D levels in black Americans have been offered as a potential explanation for some of the racial and ethnic disparities in heart disease, cancers, and other conditions." To begin to address this issue, Mayo Clinic will offer a series of informational presentations followed by question-and-answer sessions regarding the health benefits of vitamin D for black residents. "We believe it is important to pass this information to members of our Jacksonville community, and one way we can effectively do this is to go out into the community, talk to people face to face and be there to answer any questions they may have," Dr. Parker says.

ROCHESTER, Minn. — Mitochondria — subunits inside cells that produce energy — have long been thought to play a role in Alzheimer's disease. Now Mayo Clinic researchers using genetic mouse models have discovered that mitochondria in the brain are dysfunctional early in the disease. The findings appear in the journal PLoS ONE. The group looked at mitochondria in three mouse models, each using a different gene shown to cause familial, or early-onset, Alzheimer's disease. The specific mitochondria changes corresponded with the mutation type and included altered mitochondrial movement, structure, and energy dynamics. The changes happened in the brain even before the mice showed any symptoms such as memory loss. The group also found that the mitochondrial changes contributed to the later loss of mitochondrial function and the onset and progression of Alzheimer's disease. "One of the most significant findings of this study is our discovery of the impact of mitochondrial dysfunction in Alzheimer's disease," says Eugenia Trushina, Ph.D., Mayo Clinic pharmacologist and senior investigator on the study. "We are asking: Can we connect the degree of mitochondrial dysfunction with the progression of symptoms in Alzheimer's disease?" Enlisting the expertise of Mayo researcher Petras Dzeja, Ph.D., the team applied a relatively new method called metabolomics, which measures the chemical fingerprints of metabolic pathways in the cell — sugars, lipids, nucleotides, amino acids and fatty acids, for example. It assesses what is happening in the body at a given time and at a fine level of detail, giving scientists insight into the cellular processes that underlie a disease. In this case, the metabolomic profiles showed changes in metabolites related to mitochondrial function and energy metabolism, further confirming that altered mitochondrial energetics is at the root of the disease process.