…though telomerase gene therapy:
Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-‐related diseases — like osteoporosis and insulin resistance — and achieving improved readings on aging indicators like neuromuscular coordination.
The gene therapy consisted of treating the animals with a DNA-modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.
This study “shows that it is possible to develop a telomerase-based anti-aging gene therapy without increasing the incidence of cancer,” the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,” they add.
Faster, please.
If it was as simple as greater activity of a naturally occurring enzyme, why don’t we see it in the wild in mammals? There will be a side effect found, but it may be something we can live with, like increased calorie consumption.
Most mammals in the wild probably die long before they have to worry about old age. A gene that, say, lets rodents live ten times longer would offer no real evolutionary advantage if 99% of them die a violent death well before they would currently die of old age.
Faster, please.
But not with mice.