Although medical treatments have increased the average human life expectancy, these treatments have yet to increase lifespan over a hundred years. Source: Flickr

Although medical treatments have increased the average human life expectancy, these treatments have yet to increase lifespan over a hundred years. Source: Flickr

Many scientists have attmpted to find the “Fountain of Youth.” Although many genetic and medical treatments have increased the average human life expectancy, these treatments have yet to increase lifespan over a hundred years.

However, this statement may no longer hold true in the future. In a recent issue of Nature Communications, Mitra Lavasani, et al. (2012) conducted an experiment involving fast-aging, genetically engineered mice. These mice have a usual lifespan of 21 days. A few days before the mice reached their predicted maximum life span, the injections were delivered at the Institute for Regenerative Medicine in Pittsburgh. The results were astounding. The elderly mice lived approximately 70 days – three times their normal lifespan. In human terms, that would be the equivalent of an 80-year-old living to be 200.

Specifically, the investigators studied the effects of injecting muscle-derived stem/progenitor cells (MDSPCs) into a murine progeria model (fast-aging mice). Since age-related degenerative changes are universal in the musculoskeletal system, the impact on the musculoskeletal system by murine muscle-derived stem/progenitor cells (MDSPCs) became the primary focus of the experiments. MDSPCs are multipotent cells isolated from postnatal skeletal muscle. They have the capacity for long-term proliferation, are resistant to oxidative and inflammatory stress, show multilineage differentiation and self-renew, induce neovascularization, and stimulate regeneration of bone, skeletal, and cardiac muscles. These characteristics raise the possibility that the loss of MDSPCs or related perivascular progenitor cells could contribute to sarcopenia, osteoporosis and other age-associated degenerative diseases (1).

The results of Lavasani’s study indicate that MDSPC function is adversely affected by aging. Since the transplantation of functional MDSPCs was sufficient to rescue MDSPC dysfunction and extend the healthspan and lifespan of progeroid mice, investigators suspected that MDSPC dysfunction might have direct contribution to age-related degeneration.

Numerous other studies have provided evidence that the number and/or function of diverse adult stem cell populations decline with aging. However, these correlative studies do not rule out the possibility that the decline in the stem cell population have a causative role in aging.

With these results, it is reasonable to conclude that MDSPCs may have therapeutic value for delaying age-related functional decline in human progeria. It will be of great importance to test other adult stem cell types for a similar therapeutic effect (1).

This is a huge breakthrough for medicine because it will not only extend the life of humans in the future, but will also delay symptoms correlated with aging.

References:

  1. M. Lavasani et al., Nature Communications. 3, (2012).