Health & Wellbeing

“Unprecedented” research reverses age-related wrinkles and hair loss in mice

“Unprecedented” research reverses age-related wrinkles and hair loss in mice
A new study provides the first evidence that restoring mitochondrial DNA can reverse age-associated symptoms such as skin wrinkles and hair loss
A new study provides the first evidence that restoring mitochondrial DNA can reverse age-associated symptoms such as skin wrinkles and hair loss
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These images chronicle the depletion and restoration of mtDNA in a mouse experiment
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These images chronicle the depletion and restoration of mtDNA in a mouse experiment
A new study provides the first evidence that restoring mitochondrial DNA can reverse age-associated symptoms such as skin wrinkles and hair loss
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A new study provides the first evidence that restoring mitochondrial DNA can reverse age-associated symptoms such as skin wrinkles and hair loss

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More significantly, when the antibiotic trigger was withdrawn the researchers witnessed an impressive reversal of these physiological signs, including a thick regrowth of fur and a smoothing of all skin wrinkles.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.

These images chronicle the depletion and restoration of mtDNA in a mouse experiment
These images chronicle the depletion and restoration of mtDNA in a mouse experiment

"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.

Source: University of Alabama at Birmingham

3 comments
3 comments
Ralf Biernacki
We see all those miracle cures for mice---and none for humans. Why is that? Scroll a little down, and you will see a headline: "Jury awards billions to women claiming . . ." Yes, that's the reason. The risk of litigation over drug side effects is so high, and the awards so over-the-top, that it is no longer profitable, or indeed affordable, to introduce new pharmaceuticals. Most new drugs are patented and shelved, with the exception of high-profit, moderate-risk ones, like diet supplements. Unless something is done to curb this situation (like allowing patients to voluntarily waive their legal rights when receiving experimental treatments) we will never see these new, powerful drugs for cancer, aging, or degenerative diseases. Strong effective drugs are strongly bioactive, and thus by definition high risks for side effects---and consequent litigation. Mice do not sue, and mice will receive these drugs---but we will not. Take your pick: cures or lawyers. You can't have both.
Wolf0579
Yes, just let Big pharma experiment on helpless patients who then sicken and die, but we shouldn't have to pay them, they volunteered! Big money is at stake and the amount of existing profit that can be spent to insure future big profits, is huge. You saw this phenomenon in the almost year-long media blitz denouncing the Affordable Care Act, UBER-huge profits were at stake, and the medical profiteers pulled out all the stops and the largest propaganda campaign in US history kicked off.
Wolf0579
The companies that get tax breaks and still withhold products from markets in the US could find themselves nationalized under Trump.