Scientists have discovered that by changing the expression of a single gene in mice, the lifespan is increased by around 20%, according to a study published in the journal Cell Reports.
Researchers from the National Institutes of Health (NIH) conducted the study in mice, which involved targeting a gene called mTOR. The gene is linked to the balance of energy and metabolism, and now researchers believe it may be linked to increased lifespan associated with caloric restriction.
The mice were engineered to produce a level of the mTOR protein 25% lower than the normal amount, or the minimum amount needed to survive. The researchers say that although the engineered mice were smaller in size compared with control mice, they appeared to be normal.
Findings of the experiment showed that the median lifespan for the mice with reduced mTOR was 28 months for males and 31.5 months for females, compared with 22.9 months for normal male mice, and 26.5 months for normal female mice.
This increase is the equivalent of raising the average human lifespan by 16 years, from 79 to 95.
The mTOR mice also showed the greatest overall lifespans, with seven out of eight of the longest survivors being mTOR mice.
Additionally, the mice showed significant improvements in particular organs and better retention of memory and coordination when conducting maze and balance tests. The researchers add that the mTOR mice also retained more muscle, posture and strength.
The findings also revealed that the mTOR mice had a greater loss of bone volume and were more prone to infection as they got older, which means their immune function may have diminished.
Toren Finkel of the NIH’s National Heart, Lung, and Blood Institute (NHLBI) and lead researcher of the study says, however, that the change in gene expression did not affect all mice in the same way:
“While the high extension in lifespan is noteworthy, this study reinforces an important facet of aging, it is not uniform.
Rather, similar to circadian rhythms, an animal might have several organ-specific aging clocks that generally work together to govern the aging of the whole organism.”
Finkel says that these results could potentially lead to therapies for age-related diseases, such as Alzheimer’s disease, which targets specific organs.
But the researchers note that further studies are required to determine how the aging process within different tissues is connected at a molecular level.
“Our results could suggest the possibility that some interventions that slow aging may also have unintended, negative tissue-specific side effects,” they add.
“A very relevant precedent perhaps already exists for this phenomenon, as people who undergo voluntary caloric restriction appear to have a corresponding reduction in their bone mineral density.”
“Further analysis of this and related genetic models should help distinguish between these possibilities and, we hope, will help guide potential therapies aimed at extending lifespan and health span in people.”