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      Long-Term Consequences of Developmental Alcohol Exposure on Brain Structure and Function: Therapeutic Benefits of Physical Activity

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          Abstract

          Developmental alcohol exposure both early in life and during adolescence can have a devastating impact on normal brain structure and functioning, leading to behavioral and cognitive impairments that persist throughout the lifespan. This review discusses human work as well as animal models used to investigate the effect of alcohol exposure at various time points during development, as well as specific behavioral and neuroanatomical deficits caused by alcohol exposure. Further, cellular and molecular mediators contributing to these alcohol-induced changes are examined, such as neurotrophic factors and apoptotic markers. Next, this review seeks to support the use of aerobic exercise as a potential therapeutic intervention for alcohol-related impairments. To date, few interventions, behavioral or pharmacological, have been proven effective in mitigating some alcohol-related deficits. Exercise is a simple therapy that can be used across species and also across socioeconomic status. It has a profoundly positive influence on many measures of learning and neuroplasticity; in particular, those measures damaged by alcohol exposure. This review discusses current evidence that exercise may mitigate damage caused by developmental alcohol exposure and is a promising therapeutic target for future research and intervention strategies.

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          The adolescent brain and age-related behavioral manifestations.

          L Spear (2000)
          To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence.
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            The adolescent brain.

            B. J. Casey, Sarah Getz, Adriana Galvan (2008)
            Adolescence is a developmental period characterized by suboptimal decisions and actions that give rise to an increased incidence of unintentional injuries and violence, alcohol and drug abuse, unintended pregnancy and sexually transmitted diseases. Traditional neurobiological and cognitive explanations for adolescent behavior have failed to account for the nonlinear changes in behavior observed during adolescence, relative to childhood and adulthood. This review provides a biologically plausible conceptualization of the neural mechanisms underlying these nonlinear changes in behavior, as a heightened responsiveness to incentives while impulse control is still relatively immature during this period. Recent human imaging and animal studies provide a biological basis for this view, suggesting differential development of limbic reward systems relative to top-down control systems during adolescence relative to childhood and adulthood. This developmental pattern may be exacerbated in those adolescents with a predisposition toward risk-taking, increasing the risk for poor outcomes.
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              Alcohol and public health.

              Robin Room, Thomas Babor, Jürgen Rehm (2005)
              Alcoholic beverages, and the problems they engender, have been familiar fixtures in human societies since the beginning of recorded history. We review advances in alcohol science in terms of three topics: the epidemiology of alcohol's role in health and illness; the treatment of alcohol use disorders in a public health perspective; and policy research and options. Research has contributed substantially to our understanding of the relation of drinking to specific disorders, and has shown that the relation between alcohol consumption and health outcomes is complex and multidimensional. Alcohol is causally related to more than 60 different medical conditions. Overall, 4% of the global burden of disease is attributable to alcohol, which accounts for about as much death and disability globally as tobacco and hypertension. Treatment research shows that early intervention in primary care is feasible and effective, and a variety of behavioural and pharmacological interventions are available to treat alcohol dependence. This evidence suggests that treatment of alcohol-related problems should be incorporated into a public health response to alcohol problems. Additionally, evidence-based preventive measures are available at both the individual and population levels, with alcohol taxes, restrictions on alcohol availability, and drinking-driving countermeasures among the most effective policy options. Despite the scientific advances, alcohol problems continue to present a major challenge to medicine and public health, in part because population-based public health approaches have been neglected in favour of approaches oriented to the individual that tend to be more palliative than preventative.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Brain Sci
                Journal ID (iso-abbrev): Brain Sci
                Journal ID (publisher-id): brainsci
                Title: Brain Sciences
                Publisher: MDPI
                ISSN (Electronic): 2076-3425
                Publication date (Electronic): 21 December 2012
                Publication date Collection: March 2013
                Volume: 3
                Issue: 1
                Pages: 1-38
                Affiliations
                Department of Psychology, University of Delaware, Newark, DE 19716, USA; E-Mails: gillianh@ 123456psych.udel.edu (G.F.H.); kboschen@ 123456psych.udel.edu (K.E.B.)
                Author notes
                [* ] Author to whom correspondence should be addressed; E-Mail: klintsov@ 123456udel.edu ; Tel.: +1-302-831-0452; Fax: +1-302-831-3645.
                Article
                Publisher ID: brainsci-03-00001
                DOI: 10.3390/brainsci3010001
                PMC ID: 4061829
                PubMed ID: 24961305
                SO-VID: 46930d39-52fc-4398-9e59-9cb83288ab65
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 15 October 2012
                Date revision received : 01 December 2012
                Date accepted : 10 December 2012
                Categories
                Subject: Review

                Keywords: fetal alcohol,adolescence,animal model,plasticity,hippocampus,prefrontal cortex,apoptosis,neurotrophins
                Data availability:
                Keywords: fetal alcohol, adolescence, animal model, plasticity, hippocampus, prefrontal cortex, apoptosis, neurotrophins

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