Finally, Scientists Bring Hope to Mice Embarrassed by Baldness

Send in e-mailSend in e-mail
Send in e-mailSend in e-mail
A mouse with fur
A mouse with furCredit: Gil Eliahu

If left to age naturally, we wrinkle, and lose at least some hair. Both phenomena have birthed gigantic industries commensurate with our dismay. Even the ancients were sensitive about having shiny scalps: the Roman emperor Domitian, who reigned trom the year 81 to 96, famously obsessed over hair-care and wore a wig. But with all due respect to truth in advertising, nothing ever reversed this process – until now. In mice. In Alabama.

Dr. Keshav Singh of the University of Alabama and colleagues caused accelerated aging in mice; then they reversed it. They caused this by mutating a specific gene in the cell’s nuclear genome that that controls the functionality of the cellular mitochondria, they explain in a groundbreaking paper released Saturday in the Nature journal Cell Death and Disease. Mitochondria are sub-cellular structures that produce energy.

When the mitochondria were rendered dysfunctional, over the weeks of the study, the mice’s skin became increasingly wrinkled, the females more than the males, for some reason. The mice also displayed palpable loss of fur, and in the eight weeks in which they were left stewing with dysfunctional mitochondria, their skin showed signs of marked inflammation, and their movements slowed.

All are classic signs of intrinsic aging, i.e., not caused by the mice sunbathing or smoking.

Then the scientists restored mitochondrial function (by “turning off” the gene that screwed up the mitochondrial function in the first place). The mice regained their smooth skin and beautiful thick fur, to the point of becoming visually indistinguishable from normal healthy mice, the scientists say.

“To our knowledge, this observation is unprecedented,” Singh says.

The scientists hadn’t set out to cast light on the bane of baldness. The scientists had set out to investigate how mutation in mitochondrial DNA affects the “whole animal”, you or mouse.

The mitochondria are so essential to our well-being that change in them can kill us. Mutation in our mitochondrial DNA is known to cause diseases that we don’t know how to cure yet.

Irrespective of mutation, our mitochondrial function declines as we age. Scientists suspect that even diabetes, heart disease, age-related neurological disorders and even cancer may involve mitochondrial DNA depletion.

The mice actually used in the study: Before, during, after.Credit: UAB

So the scientists in Alabama engineered a mouse in which they could effectively render the mitochondria dysfunctional, then reverse the effect. They wanted to see the consequences on the body as a whole.

Lo: ubiquitous depletion of mitochondrial DNA made the mice go bald and made their skin wrinkle. Then they reversed it and lo again, the skin smoothed out and the fur grew back. Not a bad parlor trick for the very patient.

“Little change was seen in other organs when the mutation was induced, suggesting an important role for mitochondria in skin compared to other tissues,” the scientists write.

Singh himself admits to being surprised by the outcome, and suggests the mouse model could lead to drugs that augment missing mitochondrial function, to treat not only baldness and wrinkling but fatal diseases too.