‘Exercise Hormone’ Could Slow Progression of Alzheimer’s Disease

An international team of researchers led by Queen’s University, Columbia University and the Federal University of Rio de Janeiro has found that irisin, a hormone released by muscles during exercise, could slow the progression of Alzheimer’s disease.

Irisin is produced by muscles during exercise. Image credit: Free-Photos.

“In the past few years, researchers from many places around the world have shown that exercise is an effective tool to prevent different forms of dementia such as Alzheimer’s,” said study senior author Dr. Fernanda De Felice, a researcher at Queen’s University and the Federal University of Rio de Janeiro.

“This has led to an intense search for specific molecules that are responsible for the protective actions of exercise in the brain.”

“Because irisin seems to be powerful in rescuing disrupted synapses that allow communication between brain cells and memory formation, it may become a medication to fight memory loss in Alzheimer’s disease.”

Dr. De Felice and colleagues found that irisin plays an important role in the brain.

They also found irisin levels are reduced in hippocampi and cerebrospinal fluid of Alzheimer’s patients and in experimental models of the disease.

“Our study is important because curing dementia is one of the greatest current and future health care challenges,” Dr. De Felice said.

“Unfortunately, despite 30 years searching for treatment drugs, there is no effective medication for Alzheimer’s disease.”

“It is also important to remember that the vast majority of patients with dementia can be disabled due to other age-related illness (e.g. arthritis, heart disease, obesity, visual problems, and depression).”

“Furthermore, it can be challenging to engage a patient in regular physical activity.”

A drug that increases irisin in the brain could be the key.

“It is important to keep in mind that Alzheimer’s is a very complex disease and it is truly hard to treat Alzheimer’s patients before irreversible damage occurs in their brains,” Dr. De Felice said.

“This is because when a patient is diagnosed with Alzheimer’s disease, their brain has already been damaged.”

“Finding new protective routes, such as the identification of an exercise-linked component, may be an optimal strategy to heal the brain before brain cells die and dementia becomes irreversible.”

The study was published in the journal Nature Medicine.

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Mychael V. Lourenco et al. Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models. Nature Medicine 25: 165-175; doi: 10.1038/s41591-018-0275-4