Unprecedented! Scientists reverse age-related wrinkles, hair loss

When the mitochondrial function is restored by extinguishing the gene responsible for mitochondrial dysfunction, the mouse returns to Smooth and thick skin,

Scientists, including one of Indian origin, have successfully reversed hair loss and wrinkled skin – features of aging – in mice, opening the way to the treatment of related disorders at age in humans. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive and visible hair loss within a few weeks.

When mitochondrial function is restored by disabling the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age. "To our knowledge, this observation is unprecedented," said Keshav Singh, a professor at the University of Alabama in Birmingham, United States.

The mutation that does this is in a nuclear gene affecting the mitochondrial function, the tiny organelles known as the central cells. Many mitochondria in cells produce 90% of the chemical energy that cells need to survive. In humans, a decline in mitochondrial function is observed during aging, and mitochondrial dysfunction can lead to age-related diseases.

A depletion of DNA in mitochondria is also implicated in human mitochondrial diseases, cardiovascular diseases, diabetes, disorders and cancer. "This mouse model should provide an unprecedented opportunity for the development of preventive and therapeutic therapeutic strategies to increase mitochondrial functions for the treatment of cutaneous and capillary pathology associated with aging and other human diseases in which mitochondrial dysfunction play an important role."

The mutation in the mouse model is induced when doxycycline antibiotic is added to food or drinking water. This causes depletion of mitochondrial DNA as the DNA replication enzyme becomes inactive. In four weeks, the mice showed gray hair, reduced hair density, hair loss, slow motion and lethargy, changes that are reminiscent of natural aging. Wrinkled skin was observed four to eight weeks after induction of the mutation, and females had more severe skin wrinkles than males.

This hair loss and this wrinkled skin could be reversed by disabling the mutation. Little change was observed in other organs when the mutation was induced, suggesting an important role for mitochondria in the skin compared to other tissues.

Wrinkled skin showed changes similar to those observed in intrinsic and extrinsic aging. aging process, and extrinsic aging is the effect of external factors that affect aging, such as skin wrinkles that develop from excess sun or long-term smoking [19659009]. skin cells, abnormal thickening of the outer layer, dysfunctional hair follicles and increased inflammation that appears to contribute to skin pathology. These are similar to the extrinsic aging of the skin in humans.

Mice with depleted mitochondrial DNA also showed a modified expression of four age-associated markers in cells, similar to intrinsic aging. The mitochondria of mutant-induced mice have reduced mitochondrial DNA content, altered mitochondrial gene expression, and instability of large complexes in mitochondria that are involved in oxidative phosphorylation.

Inversion of the mutation restores mitochondrial function, as well as skin. capillary pathology. This shows that mitochondria are reversible regulators of skin aging and hair loss, an observation that Singh calls "surprising". It suggests that the epigenetic mechanisms underlying nuclear mitochondria play an important role in restoring normal skin. and the capillary phenotype, "said Singh