Mitochondrial DNA Could Be Key to Reversing Ageing
Researchers from the University of Alabama have identified a method by which it is possible to reduce the signs of ageing, such as wrinkles and hair loss, in mice. The technique, which was discussed in a paper in Cell Death & Disease last month, involves increasing the level of mitochondrial DNA, which declines with old age.
As our cells age, the level of mitochondrial DNA (mDNA) starts to decline and this has previously been linked to several of the physical changes associated with growing older. To mimic this process, researchers from the University of Alabama in Birmingham, USA, worked with mice whose mDNA had been artificially depleted. In reaction to the change, the mice started to lose their fur and their skin became wrinkled.
However, the team found that when they restored the mice’s mDNA levels, their skin became smooth again and their fur began to regrow.
“To our knowledge that restoration of mitochondrial functions can reverse the skin and hair pathology is unprecedented,” the authors wrote in their paper.
Importantly, the researchers noted that the reversal of ageing was very rapid; once the mDNA levels were restored (after two months of artificial depletion), the mice reverted to their original state within a month.
The research also revealed other harmful effects brought about by the mDNA depletion that were reverse once DNA levels were restored. For example, skin inflammation became worse as the concentration of white blood cells near skin cells and hair follicles increased. The team also noted that there was a consistent reduction in cell size across other organs, although this is not confirmed to have been reverse by the reintroduction of mDNA.
The authors conclude their paper by writing, “Together, this mouse model should provide an unprecedented opportunity for the development of preventative 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.”