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Is This Why We Get Old?

Mitochondrial deterioration, fueled by free radicals, may speed the aging process. But the link is far from certain.

By Rachael Moeller Gorman // Summer 2007

Mitochondrial deterioration, fueled by free radicals, may speed the aging process. But the link is far from certain.

The vicious-cycle theory of aging is also known as the mitochondrial theory, and it holds that as time passes, molecules called free radicals accumulate in the mitochondria. Free radicals are a normal result of energy production, yet they are also destructive to mitochondrial DNA. Damaged mitochondrial DNA hinders the ability of mitochondria to generate energy efficiently, causing them to churn out more polluting free radicals, which in turn cause further mitochondrial DNA damage. The theory suggests that this vicious cycle goes on in all human cells, eventually leading to sagging skin, loss of cognitive abilities and muscle decline, among other degradation.

“My mitochondrial DNA are slightly more mutated today than they were yesterday,” says neurogeneticist Nick Wood of the Institute of Neurology, University College, in London. Wood studies mutations in genes, targeting the mitochondria that result in Parkinson’s disease. “But are those mutations sufficient to cause aging, or are the mutations just a result of being on the planet for 70 years?”

Whether mitochondrial mutations actually promote aging or are coincidental—and whether free radicals even play a role—is controversial. The best study addressing the question was performed on mice in 2004 at the Karolinska Institute in Sweden. The mice had mitochondrial DNA that accumulated mutations at a faster-than-normal rate. They developed hunched backs and enlarged hearts at an early age and typically survived about half the normal life span. The researchers were able to establish a direct link between the increased mutations in mitochondrial DNA and this rapid aging, and hypothesized that free radicals were to blame. But when the same Karolinska group, using the same type of mice, repeated the experiment, this time measuring the mice’s levels of free radicals, they found the levels remained constant, making it unlikely that free radicals were the cause of premature aging.

Other studies have suggested free radicals are involved in the aging process, so it’s important to settle the debate. But if free radicals are not to blame, there’s no vicious cycle to target as a way to slow aging.


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