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      The Effects of Appropriate Perioperative Exercise on Perioperative Neurocognitive Disorders: a Narrative Review

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          Abstract

          Perioperative neurocognitive disorders (PNDs) are now considered the most common neurological complication in older adult patients undergoing surgical procedures. A significant increase exists in the incidence of post-operative disability and mortality in patients with PNDs. However, no specific treatment is still available for PNDs. Recent studies have shown that exercise may improve cognitive dysfunction-related disorders, including PNDs. Neuroinflammation is a key mechanism underlying exercise-induced neuroprotection in PNDs; others include the regulation of gut microbiota and mitochondrial and synaptic function. Maintaining optimal skeletal muscle mass through preoperative exercise is important to prevent the occurrence of PNDs. This review summarizes current clinical and preclinical evidence and proposes potential molecular mechanisms by which perioperative exercise improves PNDs, providing a new direction for exploring exercise-mediated neuroprotective effects on PNDs. In addition, it intends to provide new strategies for the prevention and treatment of PNDs.

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          Exercise as medicine - evidence for prescribing exercise as therapy in 26 different chronic diseases.

          B K Pedersen, B Saltin (2015)
          This review provides the reader with the up-to-date evidence-based basis for prescribing exercise as medicine in the treatment of 26 different diseases: psychiatric diseases (depression, anxiety, stress, schizophrenia); neurological diseases (dementia, Parkinson's disease, multiple sclerosis); metabolic diseases (obesity, hyperlipidemia, metabolic syndrome, polycystic ovarian syndrome, type 2 diabetes, type 1 diabetes); cardiovascular diseases (hypertension, coronary heart disease, heart failure, cerebral apoplexy, and claudication intermittent); pulmonary diseases (chronic obstructive pulmonary disease, asthma, cystic fibrosis); musculo-skeletal disorders (osteoarthritis, osteoporosis, back pain, rheumatoid arthritis); and cancer. The effect of exercise therapy on disease pathogenesis and symptoms are given and the possible mechanisms of action are discussed. We have interpreted the scientific literature and for each disease, we provide the reader with our best advice regarding the optimal type and dose for prescription of exercise.
          Article 0 comments Cited 748 times – based on 0 reviews     Review now
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            Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance.

            Sarah Pickles, Pierre Vigié, Richard Youle (2018)
            The maintenance of a healthy and functional mitochondrial network is critical during development as well as throughout life in the response to physiological adaptations and stress conditions. Owing to their role in energy production, mitochondria are exposed to high levels of reactive oxygen species, making them particularly vulnerable to mitochondrial DNA mutations and protein misfolding. Given that mitochondria are formed from proteins encoded by both nuclear and mitochondrial genomes, an additional layer of complexity is inherent in the coordination of protein synthesis and the mitochondrial import of nuclear-encoded proteins. For these reasons, mitochondria have evolved multiple systems of quality control to ensure that the requisite number of functional mitochondria are present to meet the demands of the cell. These pathways work to eliminate damaged mitochondrial proteins or parts of the mitochondrial network by mitophagy and renew components by adding protein and lipids through biogenesis, collectively resulting in mitochondrial turnover. Mitochondrial quality control mechanisms are multi-tiered, operating at the protein, organelle and cell levels. Herein, we discuss mitophagy in different physiological contexts and then relate it to other quality control pathways, including the unfolded protein response, shedding of vesicles, proteolysis, and degradation by the ubiquitin-proteasome system. Understanding how these pathways contribute to the maintenance of mitochondrial homeostasis could provide insights into the development of targeted treatments when these systems fail in disease.
            Article 0 comments Cited 630 times – based on 0 reviews     Review now
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              Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases.

              De-Yu Tang, Weidong Le (2016)
              One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which can be categorized into two opposite types: M1 phenotype and M2 phenotype. Depending on the phenotypes activated, microglia can produce either cytotoxic or neuroprotective effects. In this review, we focus on the potential role of M1 and M2 microglia and the dynamic changes of M1/M2 phenotypes that are critically associated with the neurodegenerative diseases. Generally, M1 microglia predominate at the injury site at the end stage of disease, when the immunoresolution and repair process of M2 microglia are dampened. This phenotype transformation is very complicated in AD due to the phagocytosis of regionally distributed β-amyloid (Aβ) plaque and tangles that are released into the extracellular space. The endogenous stimuli including aggregated α-synuclein, mutated superoxide dismutase, Aβ, and tau oligomers exist in the milieu that may persistently activate M1 pro-inflammatory responses and finally lead to irreversible neuron loss. The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit.
              Article 0 comments Cited 565 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Haipeng Zhou: hope6968@hotmail.com
                Penghui Wei:
                ORCID: http://orcid.org/0000-0003-0920-2779
                weipenghuihui@sina.com
                Journal
                Journal ID (nlm-ta): Mol Neurobiol
                Journal ID (iso-abbrev): Mol Neurobiol
                Title: Molecular Neurobiology
                Publisher: Springer US (New York )
                ISSN (Print): 0893-7648
                ISSN (Electronic): 1559-1182
                Publication date (Electronic): 19 December 2023
                Publication date PMC-release: 19 December 2023
                Publication date (Print): 2024
                Volume: 61
                Issue: 7
                Pages: 4663-4676
                Affiliations
                Department of Anesthesiology, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, ( https://ror.org/0207yh398) Qingdao, People’s Republic of China
                Author information
                http://orcid.org/0000-0003-0920-2779
                Article
                Publisher ID: 3864
                DOI: 10.1007/s12035-023-03864-0
                PMC ID: 11236851
                PubMed ID: 38110646
                SO-VID: f6466666-f77c-4899-b635-0b457b702fc2
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 12 July 2023
                Date accepted : 6 December 2023
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2024

                ScienceOpen disciplines: Neurosciences
                Keywords: exercise,perioperative neurocognitive disorders,postoperative delirium,postoperative cognitive dysfunction,mitochondria,neuroinflammation,gut microbiota
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: exercise, perioperative neurocognitive disorders, postoperative delirium, postoperative cognitive dysfunction, mitochondria, neuroinflammation, gut microbiota

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