Genetic variation in the DNA of mitochondria – the “power plants” of cells – contributes to a person’s risk of developing age-related macular degeneration (AMD), Vanderbilt investigators report May 7 in the journal PLoS ONE.
Mitochondrial genes are a logical place to expect genetic variants to influence the rate of aging. The mitochondrial DNA (mtDNA) accumulates damage and mtDNA damage is probably a major cause of aging through out the body.
The study is the first to examine the mitochondrial genome for changes associated with AMD, the leading cause of blindness in Caucasians over age 50.
“Most people don’t realize that we have two genomes,” said lead author Jeff Canter, M.D., M.P.H., an investigator in the Center for Human Genetics Research. “We have the nuclear genome – the “human genome” – that makes the cover of all the magazines, and then we also have this tiny genome in mitochondria in every cell.”
Canter teamed with Jonathan Haines, Ph.D., and Paul Sternberg, M.D., experts in AMD genetics and treatment, to examine whether a particular variation in the mitochondrial genome is associated with the disease. The genetic change occurs in about 10 percent of Caucasians, referred to as mitochondrial haplogroup T.
The tiny bit of mtDNA is much more vulnerable to damage because the mitochondria have lots of reactive chemicals in them in the process of getting converted from sugar into more useful forms of chemical energy. Some of those reactive chemicals bump into the mtDNA and cause damage that messes up energy production. But better mtDNA sequences code for mitochondrial enzymes that basically break down the sugar more cleanly with less intracellular pollution by free radicals.
Members of this team have already discovered a few other genetic variants that contribute to AMD risk.
The genetics of AMD has been a “hot” area lately, Canter said. Haines led a team that identified a variant in the Complement Factor H (CFH) gene as accounting for up to 43 percent of AMD. Variations in ApoE2 and a gene called LOC387715 on chromosome 10 have also been linked to the disease, and Haines and colleagues demonstrated an interaction between the chromosome 10 gene and smoking in raising AMD risk.
The current study also examined variation in these nuclear genes in 280 cases and 280 age-matched controls, and demonstrated that the mitochondrial genome variation was independent of the known nuclear factors.
Once cell therapy and gene therapy become practical I want to upgrade various parts of my body with stem cells that will create longer lasting tissue. We should rejuvenate our bodies. But we should also reduce the maintenance intervals. Studies such as the one above point us in the direction of how to make longer lasting components.
|Share |||Randall Parker, 2008 May 06 10:45 PM Aging Genetics|