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NEURODEGENERATION

An exercise-induced messenger boosts memory in Alzheimer’s disease

Nature Medicine volume 25, pages 20–21 (2019)Cite this article

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An exercise-linked hormone, FNDC5/irisin, mediates the benefit of exercise in Alzheimer’s disease models by enhancing synaptic plasticity and memory.

Alzheimer’s disease (AD), the most common age-related neurodegenerative disease in the world1, causes progressive brain atrophy and memory loss, leading to dementia, disability, and death. Besides the pathological hallmarks of AD—deposition of pathogenic protein aggregates such as amyloid β and tau—AD brains exhibit abnormalities of energy metabolism, such as reduced glucose uptake and insulin resistance2. AD has also been linked to peripheral metabolic changes. For example, risk for AD is increased by type 2 diabetes2 and may be reduced by metabolic disease treatment, including physical exercise3. However, the mechanism that links exercise and AD development has remained elusive. In this issue of Nature Medicine, Lourenco et al.4 report a role for the exercise-induced muscle messenger FNDC5/irisin in regulating synaptic function and memory in mouse models of AD and show that this mechanism may be relevant to humans.

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Fig. 1: Exercise-induced FNDC5/irisin prevents decline in cognitive function.

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Authors and Affiliations

  1. Gladstone Institutes, Department of Neurology, University of California San Francisco, San Francisco CA, USA

    Xu Chen & Li Gan

  2. Helen and Robert Appel Alzheimer’s Disease Research Institute, Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA

    Li Gan

Authors
  1. Xu Chen
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  2. Li Gan
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Correspondence to Li Gan.

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Competing interests

L.G is a cofounder of Aeton Therapeutics, Inc.

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Chen, X., Gan, L. An exercise-induced messenger boosts memory in Alzheimer’s disease. Nat Med 25, 20–21 (2019). https://doi.org/10.1038/s41591-018-0311-4

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  • DOI: https://doi.org/10.1038/s41591-018-0311-4

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