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      Aerobic Exercise as a Tool to Improve Hippocampal Plasticity and Function in Humans: Practical Implications for Mental Health Treatment

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          Abstract

          Aerobic exercise (AE) has been widely praised for its potential benefits to cognition and overall brain and mental health. In particular, AE has a potent impact on promoting the function of the hippocampus and stimulating neuroplasticity. As the evidence-base rapidly builds, and given most of the supporting work can be readily translated from animal models to humans, the potential for AE to be applied as a therapeutic or adjunctive intervention for a range of human conditions appears ever more promising. Notably, many psychiatric and neurological disorders have been associated with hippocampal dysfunction, which may underlie the expression of certain symptoms common to these disorders, including (aspects of) cognitive dysfunction. Augmenting existing treatment approaches using AE based interventions may promote hippocampal function and alleviate cognitive deficits in various psychiatric disorders that currently remain untreated. Incorporating non-pharmacological interventions into clinical treatment may also have a number of other benefits to patient well being, such as limiting the risk of adverse side effects. This review incorporates both animal and human literature to comprehensively detail how AE is associated with cognitive enhancements and stimulates a cascade of neuroplastic mechanisms that support improvements in hippocampal functioning. Using the examples of schizophrenia and major depressive disorder, the utility and implementation of an AE intervention to the clinical domain will be proposed, aimed to reduce cognitive deficits in these, and related disorders.

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          A neurotrophic model for stress-related mood disorders.

          There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.
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            Animal models of neuropsychiatric disorders.

            Modeling of human neuropsychiatric disorders in animals is extremely challenging given the subjective nature of many symptoms, the lack of biomarkers and objective diagnostic tests, and the early state of the relevant neurobiology and genetics. Nonetheless, progress in understanding pathophysiology and in treatment development would benefit greatly from improved animal models. Here we review the current state of animal models of mental illness, with a focus on schizophrenia, depression and bipolar disorder. We argue for areas of focus that might increase the likelihood of creating more useful models, at least for some disorders, and for explicit guidelines when animal models are reported.
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              The effects of acute exercise on cognitive performance: a meta-analysis.

              There is a substantial body of literature related to the effects of a single session of exercise on cognitive performance. The premise underlying this research is that physiological changes in response to exercise have implications for cognitive function. This literature has been reviewed both narratively and meta-analytically and, although the research findings are mixed, researchers have generally concluded that there is a small positive effect. The purpose of this meta-analysis was to provide an updated comprehensive analysis of the extant literature on acute exercise and cognitive performance and to explore the effects of moderators that have implications for mechanisms of the effects. Searches of electronic databases and examinations of reference lists from relevant studies resulted in 79 studies meeting inclusion criteria. Consistent with past findings, analyses indicated that the overall effect was positive and small (g=0.097 n=1034). Positive and small effects were also found in all three acute exercise paradigms: during exercise (g=0.101; 95% confidence interval [CI]; 0.041-0.160), immediately following exercise (g=0.108; 95% CI; 0.069-0.147), and after a delay (g=0.103; 95% CI; 0.035-0.170). Examination of potential moderators indicated that exercise duration, exercise intensity, type of cognitive performance assessed, and participant fitness were significant moderators. In conclusion, the effects of acute exercise on cognitive performance are generally small; however, larger effects are possible for particular cognitive outcomes and when specific exercise parameters are used. Copyright © 2012 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Front Hum Neurosci
                Front Hum Neurosci
                Front. Hum. Neurosci.
                Frontiers in Human Neuroscience
                Frontiers Media S.A.
                1662-5161
                29 July 2016
                2016
                : 10
                : 373
                Affiliations
                [1] 1Brain and Mental Health Lab, School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Melbourne VIC, Australia
                [2] 2Amsterdam Brain and Cognition, University of Amsterdam Amsterdam, Netherlands
                [3] 3Centre for Neuroscience, Swammerdam Institute of Life Sciences, University of Amsterdam Amsterdam, Netherlands
                Author notes

                Edited by: Claudia Voelcker-Rehage, Chemnitz University of Technology, Germany

                Reviewed by: Yvonne Nolan, University College Cork, Ireland; Dieter J. Meyerhoff, University of California, San Francisco, USA

                *Correspondence: Aaron Kandola, aaron.kandola@ 123456gmail.com Murat Yücel, murat.yucel@ 123456monash.edu
                Article
                10.3389/fnhum.2016.00373
                4965462
                27524962
                a3c886dd-5755-4531-bc6f-ce0ad0ea6527
                Copyright © 2016 Kandola, Hendrikse, Lucassen and Yücel.

                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) or licensor 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
                : 07 March 2016
                : 11 July 2016
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 401, Pages: 25, Words: 0
                Funding
                Funded by: National Health and Medical Research Council 10.13039/501100000925
                Award ID: APP1021973
                Categories
                Neuroscience
                Review

                Neurosciences
                aerobic fitness,hippocampus,plasticity,schizophrenia,depression,dementia,memory,neurogenesis
                Neurosciences
                aerobic fitness, hippocampus, plasticity, schizophrenia, depression, dementia, memory, neurogenesis

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