Review
Version 2
Preserved in Portico This version is not peer-reviewed
Does Irisin Link Physical Exercise with Alzheimer’s Disease?
Version 1
: Received: 3 December 2017 / Approved: 4 December 2017 / Online: 4 December 2017 (08:46:17 CET)
Version 2 : Received: 9 February 2018 / Approved: 11 February 2018 / Online: 11 February 2018 (04:28:07 CET)
Version 2 : Received: 9 February 2018 / Approved: 11 February 2018 / Online: 11 February 2018 (04:28:07 CET)
How to cite: Sumsuzzman, D.M.; Jin, Y.; Choi, J.; Lee, S.; Hong, Y. Does Irisin Link Physical Exercise with Alzheimer’s Disease?. Preprints 2017, 2017120023 (doi: 10.20944/preprints201712.0023.v2). Sumsuzzman, D.M.; Jin, Y.; Choi, J.; Lee, S.; Hong, Y. Does Irisin Link Physical Exercise with Alzheimer’s Disease?. Preprints 2017, 2017120023 (doi: 10.20944/preprints201712.0023.v2).
Abstract
Irisin, a skeletal muscle-secreted myokine, produced in response to physical exercise, has protective functions in both the central and the peripheral nervous systems, including the regulation of brain-derived neurotrophic factors and modification of telomere length. Such beneficial effects may inhibit or delay the emergence of neurodegenerative diseases, including Alzheimer’s disease (AD). This review is based on the hypothesis that irisin produced by physical exercise helps control AD progression. Herein, we describe the physiology of irisin and its potential role in delaying or preventing AD. Although current and ongoing studies on irisin show promising results, further research is required to clarify its potential as a meaningful therapeutic target for treating human diseases.
Subject Areas
physical exercise; irisin; neurodegeneration; aging; Alzheimer’s disease
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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