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Exercise protein may help prevent Alzheimer's memory loss

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A protein released when we exercise called irisin may help stave off memory loss associated with Alzheimer's disease, according to international scientists. After noting that levels of irisin and its precursor occur at lower levels in people with Alzheimer's, the researchers reduced the occurrence of these proteins in rodents with a model of Alzheimer's and found it caused memory deficits, while restoring the proteins reversed the deficit. They also found that if receptors for the proteins were blocked in the animals, exercise no longer benefited memory.

Journal/conference: Nature Medicine

Link to research (DOI): 10.1038/s41591-018-0275-4

Organisation/s: Federal University of Rio de Janeiro, Brazil.

Funder: Alzheimer Society of Canada, 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 and Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro, FAPERJ, CNPq, or Comissão de Aperfeiçoamento de Pessoal de Nível Superior.

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From: Springer Nature

Exercise-induced hormone may prevent Alzheimer’s-related memory loss

There may be a relationship between the exercise-induced protein hormone irisin and the progression of Alzheimer's disease, suggests a mouse study published online this week in Nature Medicine.

Exercise is known to promote beneficial health effects on numerous systems, including the brain. Previous research suggests that physical exercise may enhance cognitive abilities, and might even slow the progression of neurodegenerative disorders such as Alzheimer’s disease.

During exercise, a messenger protein called irisin can be released from muscle tissue to enter circulation and exert its effect on distant targets. Fernanda De Felice and colleagues found that irisin facilitated the pro-cognitive effects of exercise in mouse models of Alzheimer’s disease. The authors found that irisin, as well as its protein precursor FNDC5, were expressed at lower levels in the brains of humans with Alzheimer’s disease compared to healthy controls. This finding was also observed in rodent models of the disease. The authors also showed that just as learning and memory deficits were induced by reducing the genetic expression of FNDC5/irisin, restoring its expression reversed these effects in rodent models. In addition, they observed that when FNDC5/irisin signaling was blocked within the brain or peripherally in rodent models of Alzheimer’s, the pro-cognitive effects of physical exercise were lost.

Further studies are required to understand exactly how irisin enters and interacts with the brain, as well as to assess whether the protein has a similarly pro-cognitive effect in humans. However, the authors suggest that these findings may pave the way towards new therapeutic strategies to mitigate cognitive decline in patients with Alzheimer’s disease. 

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