Slowing down the dreaded aging process is something everyone is interested in, and now scientists have discovered a new way. The team discovered a feedback loop in the brain and found that increasing the activity of this circuit helped mice live longer and healthier lives. In the new study, researchers at Washington University School of Medicine in St. Louis identified a line of communication between the brain and fat stores, which play a key role in the body's energy production system.
Like many things, this connection slows down as we age, leading to some of the health problems that plague us later in life, such as weight gain.
On the bright side, the team also found that they could activate this system in mice, counteracting these negative effects, extending their lifespan and keeping them healthy longer. With more work, it might be possible to apply this to humans as well.
The breakthrough began when scientists discovered a specific group of neurons in a region of the brain called the dorsomedial hypothalamus. The study found that when these neurons are active, they produce a protein called Ppp1r17, which triggers a cascade of events that activates white fat tissue in the body. This causes the white adipose tissue to release two substances - first, the fatty acids enter the bloodstream, where they are used to provide energy for physical activity. Second, an enzyme called "ENAMPT" is released back into the hypothalamus to provide energy for brain function.
While this system works well in youth, it begins to slow down with natural aging. The team found that in older animals, Ppp1r17 leaves the neuronal nucleus and reduces the strength of its signal. Because the nervous system leading to fat tissue is less used, it shrinks over time, and the fat tissue receives fewer signals to release its molecules. This in turn leads to fat accumulation, reducing the energy available to the body.
But can this process be slowed down? To find out, the researchers activated these neurons in aged mice in two ways. One group of mice had a gene involved in this process knocked out, and another group was supplemented with more eNAMPT.
In both cases, the treated mice were more active, had fewer signs of aging (such as thinning of their coats), and lived longer than control mice. The untreated mice all died at 1,000 days (about 2.7 years), the upper limit of natural aging, but the treated mice lived 60 to 70 days longer -- an increase of about 7%.
While this approach is still a long way off in humans, the team says there is hope. If human lifespan can be extended by 7%, then for a person with a life expectancy of 75 years, it will be equivalent to about 5 more years of life. Additionally, patients stay healthy for more time.
The research was published in the journal Cell Metabolism.