UAB | Wrinkled skin and hair loss are hallmarks of aging. What if they could be reversed?
Keshav Singh, Ph.D., and colleagues have done just that, in a mouse model developed at the University of Alabama at Birmingham.
When a mutation leading to mitochondrial dysfunction is induced, the
mouse develops wrinkled skin and extensive, visible hair loss in a
matter of weeks. When the mitochondrial function is restored by turning
off 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 Singh, a professor of genetics in the UAB School of Medicine.
Importantly, the mutation that does this is in a nuclear gene
affecting mitochondrial function, the tiny organelles known as the
powerhouses of the cells. Numerous mitochondria in cells produce 90
percent of the chemical energy cells need to survive.
In humans, a decline in mitochondrial function is seen during aging,
and mitochondrial dysfunction can drive age-related diseases. A
depletion of the DNA in mitochondria is also implicated in human
mitochondrial diseases, cardiovascular disease, diabetes, age-associated
neurological disorders and cancer.
“This mouse model,” Singh said, “should provide an unprecedented
opportunity for the development of preventive 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.”
