In a mouse model developed at the University of Alabama in Birmingham, Keshav Singh, Ph.D. leads to mitochondrial dysfunction is induced; The mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks.
When mitochondrial function is restored by switching off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and dense fur that is indistinguishable from a healthy mouse of similar age
Mutation this triggers in a nuclear gene that affects mitochondrial function, the tiny organelles that are known as cell powerhouses.
In humans, a decrease in mitochondrial function is observed with increasing age, and mitochondrial dysfunctions can trigger age-related diseases. Depletion of DNA in mitochondria is also involved in human mitochondrial diseases, cardiovascular diseases, diabetes, age-related neurological disorders, and cancer.
The mutation in the mouse model is induced when the antibiotic doxycycline is added to food or drinking water. This leads to depletion of the mitochondrial DNA as the enzyme becomes inactive for replicating the DNA.
In four weeks, the mice showed gray hair, reduced hair density, hair loss, slowed movements and lethargy, changes reminiscent of natural aging. 1
A small change was observed in other organs when the mutation was induced, suggesting an important role for mitochondria in the skin compared to other tissues. The wrinkled skin showed similar changes as in the intrinsic and extrinsic skin aging – the intrinsic skin aging is the natural process of aging and extrinsic skin aging is the effect of external factors that influence skin aging, such as skin wrinkles caused by excessive sun. Long-term smoking.
Reversal of the mutation restored mitochondrial function as well as skin and hair pathology. This showed that mitochondria are reversible regulators of skin aging and hair loss, an observation that Singh calls "surprising."
The full results can be found in the journal "Cell Death and Disease"
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