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Journal ArticleDOI

Adolescent cortical development : A critical period of vulnerability for addiction

01 Feb 2007-Pharmacology, Biochemistry and Behavior (Elsevier)-Vol. 86, Iss: 2, pp 189-199
TL;DR: Findings supporting adolescence as a critical period of cortical development important for establishing life long adult characteristics that are disrupted by alcohol and drug use are presented.
Abstract: Cortical growth and remodeling continues from birth through youth and adolescence to stable adult levels changing slowly into senescence. There are critical periods of cortical development when specific experiences drive major synaptic rearrangements and learning that only occur during the critical period. For example, visual cortex is characterized by a critical period of plasticity involved in establishing visual acuity. Adolescence is defined by characteristic behaviors that include high levels of risk taking, exploration, novelty and sensation seeking, social interaction and play behaviors. In addition, adolescence is the final period of development of the adult during which talents, reasoning and complex adult behaviors mature. This maturation of behaviors corresponds with periods of marked changes in neurogenesis, cortical synaptic remodeling, neurotransmitter receptors and transporters, as well as major changes in hormones. Frontal cortical development is later in adolescence and likely contributes to refinement of reasoning, goal and priority setting, impulse control and evaluating long and short term rewards. Adolescent humans have high levels of binge drinking and experimentation with other drugs. This review presents findings supporting adolescence as a critical period of cortical development important for establishing life long adult characteristics that are disrupted by alcohol and drug use.
Citations
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Journal ArticleDOI
TL;DR: Evidence is provided that there is a heightened responsiveness to incentives and socioemotional contexts during this time, when impulse control is still relatively immature, which suggests differential development of bottom‐up limbic systems to top‐down control systems during adolescence as compared to childhood and adulthood.
Abstract: Adolescence is a developmental period characterized by suboptimal decisions and actions that are associated with an increased incidence of unintentional injuries, violence, substance 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 both childhood and adulthood. This review provides a biologically plausible model of the neural mechanisms underlying these nonlinear changes in behavior. We provide evidence from recent human brain imaging and animal studies that there is a heightened responsiveness to incentives and socioemotional contexts during this time, when impulse control is still relatively immature. These findings suggest differential development of bottom-up limbic systems, implicated in incentive and emotional processing, to top-down control systems during adolescence as compared to childhood and adulthood. This developmental pattern may be exacerbated in those adolescents prone to emotional reactivity, increasing the likelihood of poor outcomes.

2,660 citations


Cites background from "Adolescent cortical development : A..."

  • ...During early puberty, there is an overproduction of axons and synapses, followed by rapid pruning in later adolescence (Crews et al. 2007)....

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Journal ArticleDOI
TL;DR: This review will examine the relationships between impulsivity and executive function behaviors to changes in cortical structure during alcohol dependence and recovery.
Abstract: Alcohol and substance abuse disorders involve continued use of substances despite negative consequences, i.e. loss of behavioral control of drug use. The frontal-cortical areas of the brain oversee behavioral control through executive functions. Executive functions include abstract thinking, motivation, planning, attention to tasks and inhibition of impulsive responses. Impulsiveness generally refers to premature, unduly risky, poorly conceived actions. Dysfunctional impulsivity includes deficits in attention, lack of reflection and/or insensitivity to consequences, all of which occur in addiction [Evenden JL. Varieties of impulsivity. Psychopharmacology (Berl) 1999;146:348-361.; de Wit H. Impulsivity as a determinant and consequence of drug use: a review of underlying processes. Addict Biol 2009;14:22-31]. Binge drinking models indicate chronic alcohol damages in the corticolimbic brain regions [Crews FT, Braun CJ, Hoplight B, Switzer III RC, Knapp DJ. Binge ethanol consumption causes differential brain damage in young adolescent rats compared with adult rats. Alcohol Clin Exp Res 2000;24:1712-1723] causing reversal learning deficits indicative of loss of executive function [Obernier JA, White AM, Swartzwelder HS, Crews FT. Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats. Pharmacol Biochem Behav 2002b;72:521-532]. Genetics and adolescent age are risk factors for alcoholism that coincide with sensitivity to alcohol-induced neurotoxicity. Cortical degeneration from alcohol abuse may increase impulsivity contributing to the development, persistence and severity of alcohol use disorders. Interestingly, abstinence results in bursts of neurogenesis and brain regrowth [Crews FT, Nixon K. Mechanisms of neurodegeneration and regeneration in alcoholism. Alcohol Alcohol 2009;44:115-127]. Treatments for alcoholism, including naltrexone pharmacotherapy and psychotherapy may work through improving executive functions. This review will examine the relationships between impulsivity and executive function behaviors to changes in cortical structure during alcohol dependence and recovery.

615 citations


Cites background from "Adolescent cortical development : A..."

  • ...specific windows in time, during development when the environment can remodel, under genetic influences, to establish adaptive functional characteristics that persist into adulthood (Crews et al., 2007)....

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  • ...The characteristic behaviors of adolescence likely represent continued cortical development of complex functions that include sensory motor systems, but also limbic and frontal-cortical brain structures (Crews et al., 2007; Spear, 2000)....

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  • ...Studies of cortical development and function have established critical periods, e.g. specific windows in time, during development when the environment can remodel, under genetic influences, to establish adaptive functional characteristics that persist into adulthood (Crews et al., 2007)....

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  • ...This initial risk is enhanced during drinking induced cortical disruption and neurotoxicity further disrupting development of executive functions and possibly leading to persistent loss of inhibitory control (Crews et al., 2007)....

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  • ...Taken together these findings suggest that the unique developing limbic and cortical regions in adolescentbrainmaybe a critical periodof risks fordisruptionof frontalcortical development (Crews et al., 2007)....

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Journal ArticleDOI
TL;DR: The evidence supporting the link between childhood and adolescent SES and adult health is discussed, and different environmental, behavioral, and physiological pathways that might explain how early SES would influence adult health are explored.
Abstract: Socioeconomic status (SES) exposures during childhood are powerful predictors of adult cardiovascular morbidity, cardiovascular mortality, all-cause mortality, and mortality due to a range of specific causes. However, we still know little about when childhood SES exposures matter most, how long they need to last, what behavioral, psychological, or physiological pathways link the childhood SES experience to adult health, and which specific adult health outcomes are vulnerable to childhood SES exposures. Here, we discuss the evidence supporting the link between childhood and adolescent SES and adult health, and explore different environmental, behavioral, and physiological pathways that might explain how early SES would influence adult health. We also address the ages when SES exposures matter most for setting adult health trajectories as well as the role of exposure duration in SES influences on later health. While early childhood exposures seem to be potent predictors of a range of health outcomes, we emphasize that later childhood and adolescent exposures are risks for other health outcomes.

562 citations

Journal ArticleDOI
TL;DR: This article reviews the extant literature on neurocognition, brain structure, and brain function in adolescent substance users with an emphasis on the most commonly used substances, and in the context of ongoing neuromaturational processes.
Abstract: Adolescence is a unique period in neurodevelopment. Alcohol and marijuana use are common. Recent research has indicated that adolescent substance users show abnormalities on measures of brain functioning, which is linked to changes in neurocognition over time. Abnormalities have been seen in brain structure volume, white matter quality, and activation to cognitive tasks, even in youth with as little as 1-2 years of heavy drinking and consumption levels of 20 drinks per month, especially if > 4-5 drinks are consumed on a single occasion. Heavy marijuana users show some subtle anomalies too, but generally not the same degree of divergence from demographically similar non-using adolescents. This article reviews the extant literature on neurocognition, brain structure, and brain function in adolescent substance users with an emphasis on the most commonly used substances, and in the context of ongoing neuromaturational processes. Methodological and treatment implications are provided.

456 citations

Journal ArticleDOI
TL;DR: This research confirms the elevated prevalence and importance of polysubstance use behavior among adolescents prior to age 16, and puts early onset of alcohol, marijuana and cigarette use into the context of use patterns rather than single drug exposures.

387 citations

References
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Journal ArticleDOI
TL;DR: This large-scale longitudinal pediatric neuroimaging study confirmed linear increases in white matter, but demonstrated nonlinear changes in cortical gray matter, with a preadolescent increase followed by a postadolescent decrease.
Abstract: Pediatric neuroimaging studies1,2,3,4,5, up to now exclusively cross sectional, identify linear decreases in cortical gray matter and increases in white matter across ages 4 to 20. In this large-scale longitudinal pediatric neuroimaging study, we confirmed linear increases in white matter, but demonstrated nonlinear changes in cortical gray matter, with a preadolescent increase followed by a postadolescent decrease. These changes in cortical gray matter were regionally specific, with developmental curves for the frontal and parietal lobe peaking at about age 12 and for the temporal lobe at about age 16, whereas cortical gray matter continued to increase in the occipital lobe through age 20.

5,140 citations


"Adolescent cortical development : A..." refers background in this paper

  • ...At the cellular levels, these changes correspond with the marked overproduction of axons and synapses in early puberty, and rapid pruning in later adolescence (Giedd et al., 1999; Andersen et al., 2000; Andersen and Teicher, 2004)....

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  • ...Human magnetic resonance imaging (MRI) studies have demonstrated an inverted U-shape change in the gray matter volume during adolescent period, with a pre-adolescent increase followed by a post-adolescent decrease (Giedd et al., 1999; Giedd, 2004)....

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Journal ArticleDOI
TL;DR: Developmental changes 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 likely contribute to the unique characteristics of adolescence.

4,985 citations


"Adolescent cortical development : A..." refers background in this paper

  • ...Changes in reward sensitivity may reflect maturational differences in mesolimbic neural circuits (Spear, 2000; Kelley et al., 2004), which regulate the translation of motivation into action (Le Moal and Simon, 1991)....

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  • ...…defined by characteristic adolescent behaviors that include high levels of risk-taking, high exploration, novelty and sensation seeking, social interaction, high activity and play behaviors that likely promote the acquisition of the necessary skills for maturation and independence (Spear, 2000)....

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  • ...The ages associated with adolescence are commonly considered in humans to be approximately 12 to 20–25 years of age, and postnatal days (PND) 28 to 42 (Spear, 2000) in rodents....

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Journal ArticleDOI
TL;DR: The dynamic anatomical sequence of human cortical gray matter development between the age of 4-21 years using quantitative four-dimensional maps and time-lapse sequences reveals that higher-order association cortices mature only after lower-order somatosensory and visual cortices are developed.
Abstract: We report the dynamic anatomical sequence of human cortical gray matter development between the age of 4–21 years using quantitative four-dimensional maps and time-lapse sequences. Thirteen healthy children for whom anatomic brain MRI scans were obtained every 2 years, for 8–10 years, were studied. By using models of the cortical surface and sulcal landmarks and a statistical model for gray matter density, human cortical development could be visualized across the age range in a spatiotemporally detailed time-lapse sequence. The resulting time-lapse “movies” reveal that (i) higher-order association cortices mature only after lower-order somatosensory and visual cortices, the functions of which they integrate, are developed, and (ii) phylogenetically older brain areas mature earlier than newer ones. Direct comparison with normal cortical development may help understanding of some neurodevelopmental disorders such as childhood-onset schizophrenia or autism.

4,950 citations


"Adolescent cortical development : A..." refers background in this paper

  • ...Other cortical areas develop at different ages with dorsal parietal and primary sensorimotor regions showing grey matter loss at ages 4–8, and parietal areas of language and spacial orientation changing around ages 11–13 and prefrontal areas involved in integrating information from senses, reasoning and other “executive functions” maturing last during late adolescence (Gogtay et al., 2004; Toga et al., 2006)....

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  • ...…matter loss at ages 4–8, and parietal areas of language and spacial orientation changing around ages 11–13 and prefrontal areas involved in integrating information from senses, reasoning and other “executive functions” maturing last during late adolescence (Gogtay et al., 2004; Toga et al., 2006)....

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Journal ArticleDOI
25 Feb 2000-Science
TL;DR: Before the full potential of neural stem cells can be realized, the authors need to learn what controls their proliferation, as well as the various pathways of differentiation available to their daughter cells.
Abstract: Neural stem cells exist not only in the developing mammalian nervous system but also in the adult nervous system of all mammalian organisms, including humans. Neural stem cells can also be derived from more primitive embryonic stem cells. The location of the adult stem cells and the brain regions to which their progeny migrate in order to differentiate remain unresolved, although the number of viable locations is limited in the adult. The mechanisms that regulate endogenous stem cells are poorly understood. Potential uses of stem cells in repair include transplantation to repair missing cells and the activation of endogenous cells to provide "self-repair. " Before the full potential of neural stem cells can be realized, we need to learn what controls their proliferation, as well as the various pathways of differentiation available to their daughter cells.

4,608 citations