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Tracy Hampton, PhD

JAMA. 2005;294:672.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Experiments that caused mice to quickly develop characteristics of premature aging reveal that mutations in mitochondrial DNA may play a key role in growing old.

For years, mitochondria have been linked to aging. In the new findings, researchers demonstrated that an accumulation of genetic mutations in mitochondria sets off a cascade of signals that causes programmed cell death, or apoptosis (Kujoth et al. Science. 2005;309:481-484). The result is loss of irreplaceable cells and progression of aging.

A normal mouse (left) and a mouse with mitochondrial DNA defects (right) are similar in age, but the mouse at right exhibits symptoms of aging, including graying, hair loss, and loss of muscle mass and spine strength. (Photo credit: Jeff Miller/University of Wisconsin-Madison)

All mitochondria have their own DNA, separate from DNA in the cell’s nucleus. Researchers have known that mutations in mitochondrial DNA accumulate over time, but how these . . . [Full Text of this Article]