It turns out that exercise might be good for more than your waistline. A new study has found that proteins released into the brain as a result of muscular exertion cause a domino effect to occur, in which other proteins are produced and nerves and synapses are created, possibly allowing the body to postpone, or altogether prevent, the onset of neurodegenerative diseases, such as Alzheimer’s or Parkinson’s disease.
Researchers from the Dana-Farber Cancer Institute and Harvard Medical School (HMS) already knew that the protein, FNDC5, was released into the bloodstream whenever endurance exercise caused perspiration. They also knew that endurance exercise improved brain function; however, they weren’t able to connect the two. But now, they’ve discovered that increased levels of FNDC5 promotes gene expression in the hippocampus — the area associated with memory and learning — which produces a brain-protective protein, known as BDNF, Medical News Today reports.
Increased levels of BDNF in the hippocampus help preserve already existing brain cells while promoting the growth of new nerves and synapses, which are typically damaged or blocked in someone who has Alzheimer’s. Getting these processes to activate is as easy as going out for a jog, or a brisk walk, and breaking a sweat. But for those who can’t get out and exercise, the researchers have developed a way of injecting FNDC5 into the bloodstream, and tricking the body into thinking it has been exercising.
“What is exciting is that a natural substance can be given in the bloodstream that can mimic some of the effects of endurance exercise on the brain,” co-author of the study Dr. Bruce Spiegelman, of the Dana-Farber Cancer Institute and HMS, told Forbes.
Using mice, the researchers looked at these processes during 30 days of voluntary exercise on a running wheel. They then looked at whether these processes would activate when FNDC5 was injected into the bloodstream with the help of a harmless virus. Seven days after injection, they found that the mice had higher levels of BDNF in their hippocampus.
“Perhaps the most exciting result overall is that peripheral delivery of FNDC5 with adenoviral vectors is sufficient to induce central expression of BDNF and other genes with potential neuroprotective functions or those involved in learning and memory,” the authors wrote, according to Forbes.
The results of the study were significant, the researchers said. However, they cautioned that it’s too early to conclude that what worked for the mice will also work for humans. Alzheimer’s disease is the most common form of dementia, affecting an estimated five million Americans.
Previous studies have also found that exercise improves mental health. However, they did not make the connections between FNDC5 and BDNF. In July, a study found that 12 weeks of moderate exercise improved neural efficiency among adults, ages 60-88, who did and did not have mild cognitive impairment. Another study found that moderate exercise kept stress hormones — which are typically low in people with Alzheimer’s — at levels healthy enough that they were able to help protect nerves and mental health.
Source: Wrann C, Spiegelman B, Greenberg M, et al. Exercise Induces Hippocampal BDNF through a PGC-1α/FNDC5 Pathway. Cell Metabolism. 2013.