Introduction: Adolescence and young adulthood are periods of continued biological and psychosocial maturation. Thus, there may be deleterious effects of consuming large quantities of alcohol on neural development and associated cognition during this time. The purpose of this mini review is to highlight neuroimaging research that has specifically examined the effects of binge and heavy drinking on adolescent and young adult brain structure and function.

Methods: We review cross-sectional and longitudinal studies of young binge and heavy drinkers that have examined brain structure (e.g., gray and white matter volume, cortical thickness, white matter microstructure) and investigated brain response using functional magnetic resonance imaging (fMRI).

Results: Binge and heavy-drinking adolescents and young adults have systematically thinner and lower volume in prefrontal cortex and cerebellar regions, and attenuated white matter development. They also show elevated brain activity in fronto-parietal regions during working memory, verbal learning, and inhibitory control tasks. In response to alcohol cues, relative to controls or light-drinking individuals, binge and heavy drinkers show increased neural response mainly in mesocorticolimbic regions, including the striatum, anterior cingulate cortex (ACC), hippocampus, and amygdala. Mixed findings are present in risky decision-making tasks, which could be due to large variation in task design and analysis.

Conclusions: These findings suggest altered neural structure and activity in binge and heavy-drinking youth may be related to the neurotoxic effects of consuming alcohol in large quantities during a highly plastic neurodevelopmental period, which could result in neural reorganization, and increased risk for developing an alcohol use disorder (AUD).

Published in Drinking Patterns

Numerous studies have shown that alcohol intake causes neuropsychological disorders that affect various brain structures. The <> hypothesis proposes that the brain areas of alcoholics undergo deterioration similar to that observed in old age. We investigated whether alcohol abuse by young people (binge drinking) causes alterations comparable to some found in elderly people. Ninety-one people were divided into four groups: a) young people who abused alcohol; b) young people who drank alcohol in moderation; c) young people who did not drink alcohol; and d) elderly adults without any significant cognitive deterioration. All of them were assessed with a neuropsychological battery. We observed some similarities in the results obtained by young drinkers and the elderly participants, which would provide some support for the hypothesis of premature aging. The tasks that young drinkers performed worse were those related to executive functions, in which the prefrontal cortex plays an essential role. We also found differences between the two groups of young drinkers (moderate and high consumption), which leads us to believe that the amount of alcohol consumed and the pattern of consumption are factors to consider in relation to cognitive impairment.

Aims: Alcohol-dependent people who are middle-aged or older have a widespread loss of cortical grey and white matter, particularly in the prefrontal cortex (PFC). We examine if brain abnormalities are detectable in alcohol use disorders before the fifth decade (i.e. <40), and the brain structural differences associated with alcohol abuse/dependence in adolescence. Methods: Case-control studies comparing brain structure in alcohol-abusing/-dependent individuals with normal controls in which the mean age of participants was <40 were identified using Medline, EMBASE and PsychInfo. Studies in which mean age was over and under 21 were considered separately. Results: Twelve papers fulfilled inclusion criteria, five in the adolescent (14-21) and seven in the young adult age range. Two independent groups reported hippocampal and prefrontal volume reductions in adolescents, although this was consistently observed only in females. In young adults (aged 21-40), there were grey matter deficits in the PFC in both sexes. Adult women appeared to, particularly, exhibit white matter differences, evident as reduced area of the corpus callosum. Hippocampal volume reduction was observed in one study of young adults study but not another. Conclusion: The available data suggest that quantitative structural abnormalities of the brain are detectable in young alcohol abusers. There is overlap between the abnormalities seen in adolescents and young adults, although hippocampal volume loss is most consistently seen in the former group. The adolescent hippocampus may be particularly susceptible to alcohol, potentially because of an interaction between adolescent brain development and alcohol exposure

The brain is one of the major target organs of alcohol actions. Alcohol abuse can lead to alterations in brain structure and functions and, in some cases, to neurodegeneration. Cognitive deficits and alcohol dependence are highly damaging consequences of alcohol abuse. Clinical and experimental studies have demonstrated that the developing brain is particularly vulnerable to alcohol, and that drinking during gestation can lead to a range of physical, learning and behavioral defects (fetal alcohol spectrum disorders), with the most dramatic presentation corresponding to fetal alcohol syndrome. Recent findings also indicate that adolescence is a stage of brain maturation and that heavy drinking at this stage can have a negative impact on brain structure and functions causing important short- and long-term cognitive and behavioral consequences. The effects of alcohol on the brain are not uniform; some brain areas or cell populations are more vulnerable than others. The prefrontal cortex, the hippocampus, the cerebellum, the white matter and glial cells are particularly susceptible to the effects of ethanol. The molecular actions of alcohol on the brain are complex and involve numerous mechanisms and signaling pathways. Some of the mechanisms involved are common for the adult brain and for the developing brain, while others depend on the developmental stage. During brain ontogeny, alcohol causes irreversible alterations to the brain structure. It also impairs several molecular, neurochemical and cellular events taking place during normal brain development, including alterations in both gene expression regulation and the molecules involved in cell-cell interactions, interference with the mitogenic and growth factor response, enhancement of free radical formation and derangements of glial cell functions. However, in both adult and adolescent brains, alcohol damages specific brain areas through mechanisms involving excitotoxicity, free radical formation and neuroinflammatory damage resulting from activation of the innate immune system mediated by TLR4 receptors. Alcohol also acts on specific membrane proteins, such as neurotransmitter receptors (e.g. NMDA, GABA-A), ion channels (e.g. L-type Ca(2) channels, GIRKs), and signaling pathways (e.g. PKA and PKC signaling). These effects might underlie the wide variety of behavioral effects induced by ethanol drinking. The neuroadaptive changes affecting neurotransmission systems which are more sensitive to the acute effects of alcohol occur after long-term alcohol consumption. Alcohol-induced maladaptations in the dopaminergic mesolimbic system, abnormal plastic changes in the reward-related brain areas and genetic and epigenetic factors may all contribute to alcohol reinforcement and alcohol addiction. This manuscript reviews the mechanisms by which ethanol impacts the adult and the developing brain, and causes both neural impairments and cognitive and behavioral dysfunctions. The identification and the understanding of the cellular and molecular mechanisms involved in ethanol toxicity might contribute to the development of treatments and/or therapeutic agents that could reduce or eliminate the deleterious effects of alcohol on the brain.

Published in Pregnant Women


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