Adolescent Brain Development

• The developmental neuroscience of adolescence has matured in a remarkably short time, about 10 years.
• The papers in this issue show the richness, depth, and breadth of understanding that characterizes the area of developmental science.
• Mysteries, contradictions, and unknowns remain in the field.
• There is a surprising degree of consistency, consensus, and replication, given the short period of systematic study.
• Commentary focuses on broad themes across articles, regarding what is known and not known.
• Brain development study beyond expertise, commentary focuses on what new studies reveal that will be of special interest to those who study adolescent behavioral development.
• Adolescent brain differs from child and adult brains, at levels of brain structures, regions, circuits, and systems.
• Differences exist in grey matter, white matter, structural connectivity, and neurotransmission.
• Studies reveal differences in sleep, electrophysiology, functional imaging, pharmacological challenge, and stress reactivity.
• Differences consistent with studies of juvenile rodents, non-human primates, males, and females.
• They align with behavioral scientists' observations of normative development and psychopathology.
• Significant brain changes during adolescence are no longer debatable.
• Brain changes characteristic of adolescence are among the most dramatic and important to occur during the human lifespan.
• Neurobiological differences between adolescents and adults may inform how society treats young people, but such differences are real.
• "Different" does not necessarily mean "deficient", and there are important individual differences.
• Brain maturation in adolescence unfolds within an environmental context, moderating its expression in emotion, behavior, and cognition.
• There is a better understanding of how adolescent brain development may contribute to psychopathology/problem behavior than to normative development/positive functioning.

Established Principles

• Brain maturation continues through adolescence, with significant changes in prefrontal areas.
• A decline in grey matter and an increase in white matter in these regions during adolescence
• These changes aren't solely due to synaptic pruning and myelination.
• Changes in grey matter density attributed to synaptic pruning may be due to other cellular processes and white matter increases.
• The extent to which white matter alterations derive from myelin versus axonal diameter changes remains unclear.
• Density of prefrontal grey matter follows a -shaped trajectory: peaking around age 11, directs attention to studying behavioral phenomena linked to prefrontal functioning.
• Important changes occur in parietal and temporal cortices, as well as the cerebellum.
• Implications of structural changes for behavioral development are less understood than those involving the prefrontal cortex.
• Early adolescence is a time of brain plasticity, with important implications.

Brain Plasticity

• Patterns of synaptic proliferation and elimination are contextually-dependent so expect individual differences in brain structure and function linked to experience.
• Brain plasticity makes adolescence a time of considerable opportunity for intervention and may contribute to increased vulnerability to certain forms of psychopathology, many of which begin/intensify during adolescence.
• Studies show differential responsivity to stress during adolescence vs adulthood.
• Increased attention is given to changes in white matter during this period, partly stimulated by the growing use of DTI to study changes in structural connectivity.
• Adolescence is a time of dramatic changes in fiber tracts that link different brain regions and structures.
• An increase in structural connectivity is paralleled by increases in functional connectivity, with significant implications for understanding changes in adolescent behavior, especially cognitive control.
• Behavioral scientists should know that brain development in adolescence isn't all about synaptic pruning in the frontal lobe.

White Matter

• Changes in white matter are linked to changes in adolescent behavior, we will gain further insight into the neural underpinnings of behavioral development in adolescence.
• Individual differences in vulnerability to peer pressure correlate with differences in structural and functional connectivity, linking resistance to peer influence development to improvements in emotion and cognition coordination.
• Individual differences in structural connectivity during early adolescence correlate with delay discounting performance.
• Individuals with more highly organized white matter are less likely to be drawn to immediate rewards.
• Structural maturity of white matter correlates with more risk-taking.
• Research on behavioral correlates of inter-regional connectivity may prove more informative than on the correlates of grey/white matter density, especially in the study of self-regulation.
• Increases in dopaminergic activity occur during early adolescence in pathways linking limbic, striatal, and prefrontal areas.
• Animal and human studies have linked dopaminergic activity to changes in reward-directed activity.
• The pubertal period is a time of changes in appetitive behavior more generally, not simply in reward-driven behavior, as dopamine plays a role in reward anticipation/seeking and motivated action.
• Individuals are more motivated by appetitive inclinations, more oriented toward sensation-seeking, and more willing to take risks during adolescence when they must leave the natal environment/seek out mates. From an evolutionary perspective, adolescent risk-taking is a good thing.

Brain Maturation

• Changes in the ratio of grey to white matter in prefrontal areas, the increase in connectivity between prefrontal and other regions, and the increase in dopaminergic activity in prefrontal-striatal-limbic pathways provide the basis for a theory that links brain maturation in adolescence to increased vulnerability to risky behavior.
• Middle adolescence is a time of heightened vulnerability to risky/reckless behavior because of the temporal disjunction between the rapid rise in dopaminergic activity around puberty (increasing reward-seeking) and the slower maturation of the prefrontal cortex and its connections (improving cognitive control/coordination of affect/cognition).
• As dopaminergic activity declines from its early adolescent peak, and as self-regulatory systems mature, risk-taking begins to decline.
• Middle adolescence (14-17) should be a period of especially heightened vulnerability to risky behavior with high sensation-seeking and immature self-regulation.
• Many risk behaviors follow this pattern, including unprotected sex, criminal behavior, attempted suicide, and reckless driving.
• Other risky behaviors, like binge drinking, peak later as there are more constraints on opportunities to engage in them during middle adolescence.
• Adolescent brain development model has been extended beyond risk-taking in several ways.
• Adolescence is a time of important changes in processing social/emotional information, which may be linked to motivational/self-regulatory changes.
• Adolescents are highly responsive to social rewards afforded by positive peer evaluation, activating the same brain regions as non-social rewards.

Reward Processing Mediation

• Impact of peers on the neural underpinnings of risk-taking indicates peers affect risk-taking among adolescents but not adults.
• Adolescents activate socio-emotional reward regions more strongly when making risky decisions while being observed by peers than when doing so alone.
• Adults show few differences in activation of socio-emotional reward centers in the peer condition as compared to when they are alone.
• The presence of peers leads adolescents to more steeply discount delayed rewards, potentially important finding, as it provides further evidence that the impact of peers on risky decision-making may be mediated specifically by their effects on reward processing.

Psychopathology

• Many forms of psychopathology onset or intensify during adolescence that involve appetitive or affective dysregulation (e.g., depression, substance abuse, eating disorders).
• At least some forms of adolescent psychopathology are related to abnormalities in the remodeling of the dopaminergic system at puberty (which would affect appetitive/affective functioning) or in the morphological changes of the prefrontal cortex/its connections to other brain regions over adolescence (which would affect self-regulation).
• Neuroscientific model of adolescence has the potential to structure a new, overarching model of normative and atypical adolescent development.
• Early adolescence is characterized by a dramatic increase in appetitive drive, eerily similar to the basic Freudian model of adolescence.
• Increase in research on adolescent brain development during the past decade has outpaced research on the very psychological phenomena that this period of brain maturation presumably causes.
• Few studies typically include an age range spanning preadolescence, adolescence, and early adulthood because psychologists have been more interested in development during early and middle adolescence than during late adolescence or young adulthood.
• There are many behavioral and self-report studies that compare children and adolescents, fewer that compare adolescents and adults, and almost none that compare children, adolescent, and adults all at once, allow for the detection of trends that may not be linear.
• Especially problematic where reward-seeking/risk-taking are concerned due to the curvilinear nature of the developmental trajectory of dopaminergic receptor remodeling: behaviors increase until middle adolescence then decline.
• Cognitive control would be expected to increase linearly and into the decade of the 20s.
• Behavioral data on these matters comes from functional brain imaging studies of reward processing and self-regulation.
• There may be limits on how closely one can mimic real world situations in laboratory paradigms but it is possible to construct tasks that have equivalent meaning to people of different ages and, if necessary, to manipulate performance so that brain functioning can be compared both with and without equivalent performance.

Adolescent Brain

• It's important to complement neurobiological studies with experimental/field research to examine whether lab-identified principles have parallels in the real world for better understanding of adolescent behavior.
• Tested hypotheses with a large cross-sectional study of 935 individuals between the ages of 10–30.
• Reward sensitivity; preference for immediate rewards; and sensation-seeking follow a -shaped function, increasing between preadolescence and mid-adolescence, peaking between 14 and 16, and then declining.
• Impulse control; anticipation of future consequences; strategic planning; and resistance to peer influence all increase linearly from preadolescence through late adolescence and, in some respects, early adulthood.
• Model indicates individuals’ preference for risky activity, is higher during mid-adolescence than before/after, predicted independently/jointly by measures of reward-seeking and self-regulation.
• Missing from most discussions linking adolescent brain development/behavior is context.
• Neural influences are expressed with the heightened vulnerability of middle adolescence having different consequences in different settings with available opportunities to engage in reward-seeking, and with the degree to which external agents regulate adolescents whose self-regulation is still maturing.
• There are many ways for adolescents to satisfy their inclinations toward sensation-seeking that are not harmful/antisocial.
• The degree to which adolescents engage in risky behavior is in part a function of opportunities to access substances and circumstances that place them at risk.
• Brain development undoubtedly influences behavior, but it does so within a context.

Important Unanswered Questions

• The role of puberty in adolescent brain development: changes in reward-seeking are linked to the impact of gonadal hormones on brain function but the extent to which this is the case is uncertain, as is the extent to which these puberty-dependent processes differ between males/females.
• Some changes in dopaminergic activity are directly attributable to puberty's hormonal changes, some are indirectly attributable to them, and others are merely coincident with them.
• Maturation of brain systems implicated in self-regulation is independent of puberty/perhaps more contextually-dependent, but there is little research that has examined this systematically.
• The development of cognitive control is in fact experience-dependent, it is important to study which experiences matter most. Parents/educators want to know whether it is possible to facilitate the development of self-regulation.
• Exciting work is underway on the neural underpinnings of adolescent psychopathology, social cognition, and stress responsivity, and we can look forward to a dramatic increase in our understanding of these phenomena over the next decade.
• Studies of genetic influences on brain development and on brain–behavior relations in adolescence are still in their infancy, as is research on individual differences in brain development that may have genetic underpinnings.
• Research on neurotransmission is beginning to expand into other substances that may also have special significance in adolescence.
• Puberty-related increases in gonadal hormones have been linked to a proliferation of receptors for oxytocin within the limbic system.
• Excitement comes from discoveries made within laboratories of brain scientists, but the real excitement will come when this work is more fully integrated with psychological and contextual studies of this period of the life cycle.