Indian- Americal scientist, Dr Keshav Singh and his colleagues at the University of Alabama were able to reverse ageing related skin wrinkles and hair loss in mice. This is a path-breaking study and can serve as a guide for the development of drugs to reverse ageing. It was revealed that the function of mitochondria, the powerhouses of the cell is found to be the major contributor to ageing. Mitochondria account for 90 per cent of the chemical energy of all the cells.
When the scientists induced a mutation that leads to mitochondrial dysfunction, the mice developed age-related skin wrinkles and hair loss within a few weeks. However, the effects are reversed after the restoration of the mitochondrial gene. The mouse developed thick hair and smooth skin which are indicative of a healthy mouse. In humans, the function of mitochondria deteriorates with signalling the initiation of many age-related diseases. they include Diabetes, cardiovascular diseases, age-related neurovascular diseases and even Cancer.
How did they induce ageing in mice?
The team of researchers injected the mouse with an antibiotic called doxycycline. The antibiotic inactivated the enzyme responsible for the replication of the mitochondrial DNA. Soon within four weeks, there was a visible hair loss, reduced movement, the appearance of grey hair, reduction in hair density. Further within eight weeks of mutation induction, there were visible wrinkles on the skin. The wrinkled are more in female mice than the male counterparts.
Further, the wrinkled skin displayed the changes similar to intrinsic and extrinsic ageing. Intrinsic ageing is nothing but the natural process of ageing, on the other hand, extrinsic ageing is caused by physical factors such as smoking or excess sun. However, the induced mutation did not have any impact on the organs indicating the role it plays in the skin compared to other tissues. Also, the wrinkled skin displayed four age-related markers similar to intrinsic ageing.
Also, there was a visible decrease in the mitochondrial DNA content, altered mitochondrial gene expression and instability of large complexes involved in oxidative phosphorylation. Future research involves checking whether the restoration of mitochondrial genes can play any role in the reversal of phenotypic changes of organs.
The breakthrough study is published in the Journal Cell Death& Disease (2018).