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Review
. 2022 Feb:74:101543.
doi: 10.1016/j.arr.2021.101543. Epub 2021 Dec 17.

The protective role of exercise against age-related neurodegeneration

Alyson Sujkowski  1 , Luke Hong  2 , R J Wessells  3 , Sokol V Todi  4
Affiliations
Review

The protective role of exercise against age-related neurodegeneration

Alyson Sujkowski et al. Ageing Res Rev. 2022 Feb.

Abstract

Endurance exercise is a widely accessible, low-cost intervention with a variety of benefits to multiple organ systems. Exercise improves multiple indices of physical performance and stimulates pronounced health benefits reducing a range of pathologies including metabolic, cardiovascular, and neurodegenerative disorders. Endurance exercise delays brain aging, preserves memory and cognition, and improves symptoms of neurodegenerative pathologies like Amyotrophic Lateral Sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, and various ataxias. Potential mechanisms underlying the beneficial effects of exercise include neuronal survival and plasticity, neurogenesis, epigenetic modifications, angiogenesis, autophagy, and the synthesis and release of neurotrophins and cytokines. In this review, we discuss shared benefits and molecular pathways driving the protective effects of endurance exercise on various neurodegenerative diseases in animal models and in humans.

Keywords: Exercise; Mitochondria; Muscle; Neurodegeneration; Proteinopathy.

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Conflict of interest statement

Conflicts of Interest: The authors declare that they do not have any conflicts of interest to disclose.

Figures

Fig 1:
Fig 1:. Summary of exercise effects on ALS.
Detailed description of data from animal models is in Table 1. Detailed description of data from human studies is in Table 2.
Fig 2:
Fig 2:. Summary of exercise effects on AD.
Detailed description of data from animal models is in Table 1. Detailed description of data from human studies is in Table 2. Abbreviations: BDNF-brain derived neurotrophic factor, DA-dopamine, DAT-dopamine uptake transporter, DJ-1-protein deglycase DJ-1, GDNF-glial derived neurotrophic factor, Hsp70-Heat shock protein 70kD, TNFα-tumor necrosis factor alpha, SOD-superoxide dismutase.
Fig 3:
Fig 3:. Summary of exercise effects on PD.
Detailed description of data from animal models is in Table 1. Detailed description of data from human studies is in Table 2. Abbreviations: BACE-β-site amyloid precursor protein cleaving enzyme 1, BDNF-brain derived neurotrophic factor, IL-10-interleukin 10, Nrf2-nuclear factor erythroid 2–related factor 2, TNFα-tumor necrosis factor alpha.
Fig 4:
Fig 4:. Summary of exercise effects on HD.
Detailed description of data from animal models is in Table 1. Detailed description of data from human studies is in Table 2. Abbreviations: Bax-Bcl-like protein 4, Bcl-2-B cell lymphoma protein 2.
Fig 5:
Fig 5:. The polyQ family of neurodegenerative diseases.
The nine known polyQ diseases are listed along with their causative proteins, the protein’s relative size compared to other polyQ disease proteins and their putative functions. Boxed region in SCA6 indicates transcription factor encoded by α1A-CT. Red bars represent the relative location of the polyQ repeat in each protein, and red arrows indicate the range of repeat lengths associated with disease. Whereas CAG/polyQ repeat length is generally stable in an individual (with modest somatic mosaicism), repeat length often changes size in successive generations of a family (Williams and Paulson, 2008). Abbreviations: DRPLA = dentatorubral-pallidoluysian atrophy; HD = Huntington’s disease; SBMA = spinobulbar muscular atrophy; SCA = spinocerebellar ataxia.
Fig 6:
Fig 6:. Summary of exercise effects on polyQ SCAs.
Detailed description of data from animal models is in Table 1. Detailed description of data from human studies is in Table 2. Abbreviations: EGF-epidermal growth factor receptor, phosphor-rpS6-phophorylated ribosomal protein S6, TFEB-transcription factor EB. Figures 1–4, 6 created with BioRender.com
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