A hormone released during exercise, Irisin, may protect the brain against Alzheimer’s disease, and explain the positive effects of exercise on mental performance. In mice, learning and memory deficits were reversed by restoring the hormone. People at risk could one day be given drugs to target it. : Health

The title of the post is a copy and paste from the first, third and fifth paragraphs of the linked academic press release here:

A hormone released during exercise may protect the brain against Alzheimer’s disease. It may also explain the known positive effects of exercise on mental performance.

In tests with mice, the team could induce learning and memory deficits by cutting out irisin and could reverse the effects by restoring the hormone.

Some people who are unable to regularly exercise but have dementia or are at high risk of dementia could one day be given drugs to to target irisin.

Journal Reference:

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

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

Nature Medicine, volume 25, pages165–175 (2019)

DOI: https://doi.org/10.1038/s41591-018-0275-4

Link: https://www.nature.com/articles/s41591-018-0275-4

Abstract

Defective brain hormonal signaling has been associated with Alzheimer’s disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.

Source link