An exercise-linked hormone known as irisin that could slow the progression of Alzheimer’s disease, reports Queen’s University researcher Fernanda De Felice, along with co-authors from the Federal University of Rio de Janeiro.
The findings demonstrate that the hormone, which is boosted by exercise, plays an important role in the brain and that Alzheimer patients carry less of the hormone. This discovery brings science one step closer to developing a medication that reproduces the effects of exercise-induced irisin production in the brain.
“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. 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,”
says Dr. De Felice, a researcher in the Centre for Neuroscience Studies at Queen’s.
The new research is significant, explains Dr. De Felice, as curing dementia is one of the greatest current and future health care challenges. Unfortunately, despite 30 years searching for treatment drugs, there is no effective medication for Alzheimer’s disease.
She adds it is also important to remember that the vast majority of patients with dementia can be disabled due to other age-related conditions, such as 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.
Very Complex Disease
The next step in Dr. De Felice’s research is investigating the most effective way of delivering irisin to the brain.
“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. 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,”
Dr. De Felice says.
The research was supported by grants from Alzheimer Society of Canada and the Weston Brain Institute, National Institute for Translational Neuroscience, Human Frontier Science Program, International Society for Neurochemistry, National Institutes of Health, Canadian Institutes of Health Research, and from the Brazilian funding agencies Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro.
Mychael V. Lourenco, Rudimar L. Frozza, Guilherme B. de Freitas, Hong Zhang, Grasielle C. Kincheski, Felipe C. Ribeiro, Rafaella A. Gonçalves, Julia R. Clarke, Danielle Beckman, Agnieszka Staniszewski, Hanna Berman, Lorena A. Guerra, Letícia Forny-Germano, Shelby Meier, Donna M. Wilcock, Jorge M. de Souza, Soniza Alves-Leon, Vania F. Prado, Marco A. M. Prado, Jose F. Abisambra, Fernanda Tovar-Moll, Paulo Mattos, Ottavio Arancio, Sergio T. Ferreira & Fernanda G. De Felice
Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models
Nature Medicine volume 25, pages 165–175 (2019)