How exercise may help reduce the risk of Alzheimer’s disease

New research is providing more evidence as to the effectiveness of physical exercise in those at risk of developing long-term cognitive impairments, like Alzheimer’s disease.

According to a study, irisin, a hormone produced in the body after strenuous exercise, might protect neurons combating the neurodegenerative disease. In previous studies, exercise researchers uncovered the efficiency of the hormone in increasing memory and energy metabolism. Upon the newest findings, researchers now believe it may also promote neuronal growth in the hippocampus, a region of the brain vital for learning and memory.

Ottavio Arancio, M.D., along with researchers at the Federal University of Rio de Janeiro in Brazil and Queens University in Canada, investigated a possible link between irisin and Alzheimer’s in humans. The study was led by Arancio, and others, at Columbia University’s Vagelos College of Physicians and Surgeons and Taub Institute for Research on Alzheimer’s Disease and the Aging Brain.

They observed irisin in the hippocampus and reduced levels of the hormone in this region among patients with the neurodegenerative illness, the team found.

To further study the hormone’s role in the brain, researchers ran various experiments on mice. The experiments showed that irisin protects the brain’s synapses and memory. Both synapses and memory weakened however when irisin was not present in the hippocampus of healthy mice. Increasing irisin in the brain led to improved brain health in both of these measures.

The team then turned to probe physical exercise and its effect on irisin. In experiments initiated on mice, it was found that daily swimming activities lasting no less than five weeks inhibited the development of memory deficits, this was despite infusions of beta-amyloid, a protein linked to Alzheimer’s.

In mice who were treated with irisin-blocking substances, the benefits of swimming were eliminated and had similar memory performance compared to sedentary animals after infusions with beta-amyloid, the study found.

The findings point to irisin for potential in the creation of better therapy against dementia in humans.

“In the meantime, I would certainly encourage everyone to exercise, to promote brain function and overall health,” said Arancio. “But that’s not possible for many people, especially those with age-related conditions like heart disease, arthritis, or dementia. For those individuals, there’s a particular need for drugs that can mimic the effects of irisin and protect synapses and prevent cognitive decline.”

The findings were published in the journal Nature Medicine.