An exercise-induced hormone linked to a range of benefits might add another to its repertoire: protection against Alzheimer’s disease.
A new paper, published in Nature Medicine, explains that the hormone irisin, released by our bodies when we exert ourselves, seems to offer protection against the memory loss and brain damage associated with Alzheimer’s. In those with the disease, however, irisin levels are depleted. Boosting irisin levels through exercise, then, might be a way to stave off the disease.
Irisin gets released into our bodies when we use our muscles, and it helps convert fat into heat and energy. This newly-discovered function for the hormone expands its known uses into the mind, and might help explain why lifestyle factors like exercise seem to help slow the progression of Alzheimer’s.
The results offer new hope for human patients and their families waiting for an Alzheimer’s cure, said Ottavio Arancio, a researcher at Columbia University, who conducted the study in collaboration with an international team of scientists.
“Our study demonstrates that irisin mediates the beneficial impact of exercise on memory, and offers a novel explanation for how regular exercise may reduce the risk of developing Alzheimer’s disease and why exercise appears to be beneficial for patients at early stages of memory loss,” Arancio said.
The team first looked for the presence of the hormone in brain bank tissue samples. They observed irisin in the human hippocampus and found that levels of the hormone were depleted in brains that were afflicted with Alzheimer’s.
Next, the team studied how irisin affects the brain using lab mice. They found that mice who swam every day over the course of five weeks did not develop memory problems despite receiving infusions of beta-amyloid — a sticky and clumpy brain protein implicated in Alzheimer’s disease.
The researchers also treated mice that swam with an irisin-blocking drug. This eliminated the cognitive benefits of swimming. These mice performed no better on memory tests than sedentary mice after being infused with beta-amyloid.
Together, the findings position irisin as a possible new compound for preventing or treating Alzheimer’s and other forms of dementia in humans, Arancio said.
However, the study left researchers with some unanswered questions to clear up before a therapy gets off the drawing board. For instance, the underlying mechanisms of irisin’s protective effects aren’t fully understood. It is also unclear whether irisin, which is produced by muscles, is circulated to the brain or if exercise promotes irisin expression in the brain itself.
But for now, Arancio says irisin holds promise in the fight against Alzheimer’s — whether boosted naturally through exercise or as a new drug therapy in the future.
“Exercise may be an optimal strategy to ward off dementia. On the other hand, it is important to find effective medications for patients who no longer can exercise adequately,” Arancio said. “Because irisin is a molecule naturally produced by the human organism, it is conceivable that side effects of a potential treatment based on irisin would be reduced.”
Next, the team will determine whether the beneficial effects of irisin observed in mice will translate to non-human primate brains.