Beating ageing just got a leg-up—a team of researchers at the University of Edinburgh have successfully reversed its effects on the thymus in live elderly mice, the BBC has reported. They did this rebooting a single gene, Foxn1, that naturally shuts down with age causing the thymus to shrink. The thymus is critical to the adaptive immune system in vertebrates—T-cells, that are part of both immunological memory and acquired immune response, mature here. However, the effects of age on the thymus are rather drastic—in a 70-year-old person, it might be as much as ten times smaller than it is in an adolescent. Consequently, as a person ages, she becomes more susceptible to recurring infections. The Edinburgh team used a drug to reactivate Foxn1 in the test mice and observed the rejuvenation of the thymus. As the gene’s activity increased, the thymus’s size and level of T-cell production approached what is seen in much younger mice.
While the findings are significant for immunology, the bigger impact therein is for regenerative biology. It is the first instance of the successful manipulation of a single protein to restart an organ that age shuts down. And given the test subject is a mammal, we are a step closer to replicating the same in humans. Perfecting the control of a single gene in a live animal opens up the possibility of similar control of genes that are responsible for, say, the heart or the brain, organs on which the effects of the ageing process are more manifest. The possibilities are quite exciting for the brain, especially—progresses in regenerative biology could one day help reverse senile
dementia, or even Alzheimer's.