A breakthrough new study from researchers at University of Alabama at Birmingham has demonstrated that reversing mitochondrial dysfunction in mouse models can reverse hair loss and smooth wrinkles. The research points to new targets for scientists to investigate in developing treatments for age-related skin deterioration and hair loss.

For some time, researchers have identified a correlation between aging and a decline in mitochondrial function. Depletion of mitochondrial DNA (mtDNA) has been implicated in a number of human diseases, including diabetes, age-associated neurological disorders, and even cancer.

It has been estimated that, on average, a human loses four copies of mtDNA every decade. Whether this decrease in mtDNA is causally connected to age-related disease is still a topic of debate but this new study effectively demonstrates for the first time that restoration of mtDNA can improve a number of age-associated physiological pathologies.

The new study began by engineering a mouse model where mtDNA can be depleted using a common antibiotic trigger. At eight weeks of age the mice were administered the antibiotic trigger, resulting in a subsequent depletion of mtDNA. Within four weeks the mice displayed hair loss, wrinkled skin and lethargy, all signs of natural aging, albeit in an accelerated fashion.

More significantly, when the antibiotic trigger was withdrawn the researchers witnessed an impressive reversal of these physiological signs, including a thick regrowth of fur and a smoothing of all skin wrinkles. This dramatic reversal surprised the researchers, with the study suggesting for the first time that mtDNA could be an effective regulator of skin aging and hair loss.

"To our knowledge, this observation is unprecedented," says Keshav Singh, one of the authors on the study. "It suggests that epigenetic mechanisms underlying mitochondria-to-nucleus cross-talk must play an important role in the restoration of normal skin and hair phenotype."

The study didn't examine broader systemic repercussions from this specific kind of depletion and restoration of mtDNA, but initial examinations saw few changes in the animals' other organs, suggesting mitochondria play a very important role in skin compared to other tissues in the body.

Of course, a great deal more research needs to be done before this discovery results in an actionable human treatment, but if this direct mechanism can be replicated in humans, and effectively modulated, then it may offer a future where we can reduce age-related physiological degeneration such as wrinkling and hair loss.

"This mouse model should provide an unprecedented opportunity for the development of preventive and therapeutic drug development strategies to augment the mitochondrial functions for the treatment of aging-associated skin and hair pathology and other human diseases in which mitochondrial dysfunction plays a significant role," says Singh.

The research was published in the journal Cell Death and Disease.

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