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      Protective effect of irisin against Alzheimer’s disease

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          Abstract

          Despite being one of the greatest global challenges for health and social care in the 21st century, Alzheimer’s disease (AD) lacks specific medicine. Irisin, an exercise-generated muscle factor, emerges as a potential hormone for AD prevention and treatment because of its role in promoting the browning of white adipose tissue, accelerating energy expenditure, regulating energy metabolism, and improving insulin resistance. The study reviews classic hallmarks of AD and irisin’s physiology before discussing the possible mechanism by which irisin protects against AD in terms of its effects related to molecular biology and cellular biology. Results reveal that irisin sharpens learning memory by inducing the production of brain-derived neurotrophic factor (BDNF), lowers the production of inflammatory factors, protects neurology through astrocytes, and ameliorates AD symptoms by improving insulin resistance. The review aims to facilitate future experimental studies and clinical applications of irisin in preventing and treating AD.

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          Alzheimer Disease: An Update on Pathobiology and Treatment Strategies

          Justin M. Long, David Holtzman (2019)
          Alzheimer disease (AD) is a heterogeneous disease with a complex pathobiology. The presence of extracellular amyloid-β deposition as neuritic plaques and intracellular accumulation of hyperphosphorylated tau as neurofibrillary tangles remain the primary neuropathologic criteria for AD diagnosis. However, a number of recent fundamental discoveries highlight important pathological roles for other critical cellular and molecular processes. Despite this, no disease modifying treatment currently exists and numerous phase 3 clinical trials have failed to demonstrate benefit. We review here recent advances in our understanding of AD pathobiology and discuss current treatment strategies, highlighting recent clinical trials and opportunities for developing future disease modifying therapies.
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            A PGC1α-dependent myokine that drives browning of white fat and thermogenesis

            Pontus Boström, Yao-jun Wu, Mark P. Jedrychowski … (2012)
            Exercise benefits a variety of organ systems in mammals, and some of the best-recognized effects of exercise on muscle are mediated by the transcriptional coactivator PGC1α Here we show that PGC1α expression in muscle stimulates an increase in expression of Fndc5, a membrane protein that is cleaved and secreted as a new hormone, irisin. Irisin acts on white adipose cells in culture and in vivo to stimulate UCP1 expression and a broad program of brown fat-like development. Irisin is induced with exercise in mice and humans, and mildly increased irisin levels in blood cause an increase in energy expenditure in mice with no changes in movement or food intake. This results in improvements in obesity and glucose homeostasis. Irisin could be a protein therapeutic for human metabolic disease and other disorders that are improved with exercise.
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              Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway.

              Christiane D Wrann, James P. White, John Salogiannnis … (2013)
              Exercise can improve cognitive function and has been linked to the increased expression of brain-derived neurotrophic factor (BDNF). However, the underlying molecular mechanisms driving the elevation of this neurotrophin remain unknown. Here we show that FNDC5, a previously identified muscle protein that is induced in exercise and is cleaved and secreted as irisin, is also elevated by endurance exercise in the hippocampus of mice. Neuronal Fndc5 gene expression is regulated by PGC-1α, and Pgc1a(-/-) mice show reduced Fndc5 expression in the brain. Forced expression of FNDC5 in primary cortical neurons increases Bdnf expression, whereas RNAi-mediated knockdown of FNDC5 reduces Bdnf. Importantly, peripheral delivery of FNDC5 to the liver via adenoviral vectors, resulting in elevated blood irisin, induces expression of Bdnf and other neuroprotective genes in the hippocampus. Taken together, our findings link endurance exercise and the important metabolic mediators, PGC-1α and FNDC5, with BDNF expression in the brain. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Psychiatry
                Journal ID (iso-abbrev): Front Psychiatry
                Journal ID (publisher-id): Front. Psychiatry
                Title: Frontiers in Psychiatry
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-0640
                Publication date (Electronic): 20 September 2022
                Publication date Collection: 2022
                Volume: 13
                Electronic Location Identifier: 967683
                Affiliations
                [1] 1Tianjin Key Lab of Exercise Physiology and Sports Medicine, Tianjin University of Sport , Tianjin, China
                [2] 2Institute of Environmental and Operational Medicine, Academy of Military Medicine Sciences, Academy of Military Sciences , Tianjin, China
                Author notes

                Edited by: Rajesh Tampi, Creighton University, United States

                Reviewed by: Saeid Taheri, University of South Florida, United States; Cyle Johnson, Creighton University, United States

                *Correspondence: Kun Wang, wangk09@ 123456qq.com

                This article was submitted to Aging Psychiatry, a section of the journal Frontiers in Psychiatry

                Article
                DOI: 10.3389/fpsyt.2022.967683
                PMC ID: 9530446
                PubMed ID: 36203845
                SO-VID: 1e582c53-8bff-4639-a97c-7838d99eb87a
                Copyright © Copyright © 2022 Chen, Wang and Wang.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 13 June 2022
                Date accepted : 29 August 2022
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 61, Pages: 8, Words: 5985
                Categories
                Subject: Psychiatry
                Subject: Review

                ScienceOpen disciplines: Clinical Psychology & Psychiatry
                Keywords: irisin,alzheimer’s disease,bdnf,neuroprotection,neuroinflammation
                Data availability:
                ScienceOpen disciplines: Clinical Psychology & Psychiatry
                Keywords: irisin, alzheimer’s disease, bdnf, neuroprotection, neuroinflammation

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