A new study has revealed a compelling association between a hormone released during exercise and the prevention of neurodegeneration seen in conditions such as Alzheimer's disease. The research in mice suggests the exercise-induced hormone irisin may improve brain plasticity and memory, helping explain how exercise confers beneficial effects on brain health.

While we know exercise is important for cardiovascular and physical health there is still some debate over how beneficial it is in slowing or reversing the progression of dementia and Alzheimer's disease. Studies have certainly found, for young healthy adults, exercise can directly enhance brain health and cognition. But can exercise slow the progress of dementia in older adults already suffering progressive cognitive decline?

Despite strong epidemiological associations linking increased physical activity to a reduced risk of Alzheimer's disease, more direct clinical trials have reported mixed results. Perhaps the most rigorous randomized control trial, involving nearly 500 people, published its controversial results last year, concluding moderate to high intensity exercise does not slow the progression of dementia. Even more concerning was the trial's suggestion that some types of exercise may even worsen the progression of cognitive impairment.

Experts suggest that the discordancy in different study conclusions points to a growing problem in dementia research. Many prospective treatments may be incredibly promising in terms of preventing the onset of dementia and Alzheimer's, however, once the cognitive damage has taken hold these treatments may be ineffective.

A new study is attempting to home in on the biological mechanisms at play in the relationship between exercise and cognition. The research first revealed that irisin, a hormone upregulated by exercise and released by muscles during exertion, is significantly reduced in the hippocampus and central nervous system of late-stage human Alzheimer's disease patients and animal models engineered with the disease.

The study then artificially impaired irisin levels in the brains of normal mice resulting in reductions in synaptic plasticity and memory. Boosting irisin levels in mice engineered with Alzheimer's also demonstrated notable improvements in synaptic plasticity and memory.

Even more interestingly it was found that inhibiting irisin in the brain of Alzheimer's modeled mice resulted in a blocking of the beneficial effects of exercise. The Alzheimer's mice without the irisin-block revealed daily exercise slowed, or even protected, from synaptic degeneration. This suggests that exercise can prevent, or at least slow, the onset of neurodegeneration through an intriguing muscle-to-brain axis mediated by irisin.

It is still early days for the research, and there are plenty of questions that remain unanswered. Does irisin confer these same pro-cognitive effects in humans? How exactly does the hormone move from muscles into the brain? And what mechanism does it specifically trigger in the brain to help protect against dementia-related neurodegeneration?

Nevertheless, this is an intriguing new discovery that may ultimately help direct researchers towards new treatments for aging patients unable to engage in functional levels of physical exercise.

The new study was published in the journal Nature Medicine.