Due to an immature prefrontal cortex, adolescents also have an increased sex drive and problems in self-regulation as illustrated in this flow diagram.
MRI studies have discovered that developmental processes tend to occur in the brain in a back-to-front pattern, explaining why the prefrontal cortex develops last.
These studies have also shown that teens have less white matter myelin in the frontal lobes compared to adults, and that myelin in the frontal lobes increases throughout adolescence. During adolescence, white matter increases in the corpus callosum, the bundle of nerve fibers connecting the right and left hemispheres of the brain, which allows for efficient communication between the hemispheres and enables an individual to access a full array of analytical and creative strategies to respond to complex dilemmas that may arise in adolescent life.
Hence, the role of experience is critical in developing the neurocircuitry that allows for increased cognitive control of the emotions and impulses of adolescence.
Adolescents, who tend to engage in risky behaviors in relatively safe environments, utilize this circuitry and develop the skills to tackle more dangerous situations; however, with an immature prefrontal cortex, even if adolescents understand that something is dangerous, they may still engage in such risky behavior.
The exact biological basis of risk-taking behavior in adolescents remains enigmatic. Adolescents are at their peak of physical strength, resilience, and immune function, yet mortality rates among 15—24 year olds are more than triple the mortality rates of middle school children.
The Centers for Disease Control and Prevention has identified the leading causes of death and illness among adolescents, 22 , 23 , 59 as illustrated in Figure 5. It is generally held that adolescents take risks to test and define themselves, as risk-taking can be both beneficial and harmful. It can lead to situations where new skills are learned and new experiences can prepare them for future challenges in their lives.
Risk-taking serves as a means of discovery about oneself, others, and the world at large. The proclivity for risk-taking behavior plays a significant role in adolescent development, rendering this a period of time for both accomplishing their full potential and vulnerability.
Hence, acquiring knowledge regarding adolescent brain maturation can help understand why teens take risks, while keeping in mind that risk-taking behavior is a normal and necessary component of adolescence. This knowledge may help in developing physiologically and pharmacologically effective interventions that focus on reducing the negative consequences associated with risk-taking behavior among the adolescent population.
Notes: Injury and violence are the two most common leading causes of death during adolescence. It has been established that, around the age of 12 years, adolescents decrease their reliance on concrete thinking and begin to show the capacity for abstract thinking, visualization of potential outcomes, and a logical understanding of cause and effect.
Teens were found to be capable of reasoning about the possible harm or benefits of different courses of action; however, in the real world, teens still engaged in dangerous behaviors, despite understanding the risks involved. Under these conditions, teens tend to make poorer decisions. The opposite of hot cognition is cold cognition, which is critical and over-analyzing. Then, with the addition of complex feelings — such as fear of rejection, wanting to look cool, the excitement of risk, or anxiety of being caught — it is more difficult for teens to think through potential outcomes, understand the consequences of their decisions, or even use common sense.
Brain imaging has shown that the nucleus accumbens is highly sensitive in adolescents, sending out impulses to act when faced with the opportunity to obtain something desirable.
These changes are related to decreases in DA, a neurotransmitter that produces feelings of pleasure. Self-regulation has been broadly classified as the management of emotions and motivation. Self-regulation also entails controlling the expression of intense emotions, impulse control, and delayed gratification. As adolescents progress toward adulthood with a body that is almost mature, the self-regulatory parts of their brains are still maturing.
An earlier onset of puberty increases the window of vulnerability for teens, making them more susceptible to taking risks that affect their health and development over a prolonged period. Behavioral control requires a great involvement of cognitive and executive functions.
These functions are localized in the prefrontal cortex, which matures independent of puberty and continues to evolve up until 24 years of age. It has been suggested that, during this period, adolescents should not be overprotected, but be allowed to make mistakes, learn from their own experiences, and practice self-regulation. Parents and teachers can help adolescents through this period by listening and offering support and guidance.
Recently, Steinberg studied risk-taking behavior in teens and how this was influenced by their peers. When teens find themselves in emotionally arousing situations, with their immature prefrontal cortices, hot cognitive thinking comes into play, and these adolescents are more likely to take riskier actions and make impulsive decisions. Mass media, community, and adult role models can also influence adolescent risk-taking behaviors.
Teens are constantly exposed to emotionally arousing stimuli through multimedia, which encourages unprotected sex, substance abuse, alcohol abuse, and life-threatening activities. Even adults can have trouble resisting engaging in some of these risky behaviors; however, the temptation must be much harder for teens, whose judgment and decision-making skills are still developing.
Recent functional MRI studies have demonstrated the extent of development during adolescence in the white matter and grey matter regions within the social brain. Activity in some of these regions showed changes between adolescence and adulthood during social cognition tasks.
These studies have provided evidence that the concept of mind usage remains developing late in adolescence. The mechanisms underlying the long-term effects of prenatal substance abuse and its consequent elevated impulsivity during adolescence are poorly understood. Liu and Lester 34 have reported on developmentally-programmed neural maturation and highlighted adolescence as a critical period of brain maturation.
These investigators have studied impairments in the DAergic system, the hypothalamic—pituitary—adrenal axis, and the pathological interactions between these two systems that originate from previous fetal programming in order to explain insufficient behavioral inhibition in affected adolescents.
In addition, Burke 35 has examined the development of brain functions and the cognitive capabilities of teenagers. Specifically, these two sets of investigators have explored the effect of alcohol abuse on brain development, and the fundamental cognitive differences between adolescents and adults, and have suggested that the adultification of youth is harsh for those whose brains have not fully matured. Cannabis is the most commonly consumed drug among adolescents, and its chronic use may affect maturational refinement by disrupting the regulatory role of the endocannabinoid system.
In animals, adolescent cannabinoid exposure caused long-term impairment in specific components of learning and memory, and differentially affected emotional reactivity with milder effects on anxiety behavior and more pronounced effects on depressive behavior. So far, only a few studies have investigated the neurobiological substrates of this vulnerability; 56 hence, further investigation is required to clarify the molecular mechanisms underlying the effect of cannabis on the adolescent brain.
Recent studies have provided a neural framework to explain the developmental differences that occur within the mesolimbic pathway based on the established role of DA in addiction. DAergic pathways originate in the ventral tegmental area and terminate in the nucleus accumbens, where dopamine is increased by nicotine, but decreased during withdrawal.
Thus, it has been hypothesized that adolescents display enhanced nicotine reward and reduced withdrawal via enhanced excitation and reduced inhibition of ventral tegmental area cell bodies that release DA in the nucleus accumbens. Adolescents that initiate tobacco abuse are more vulnerable to long-term nicotine dependence. A unifying hypothesis has been proposed based on animal studies, and it suggests that adolescents as compared to adults experience enhanced short-term positive effects and reduced adverse effects toward nicotine, and they also experience fewer negative effects during nicotine withdrawal.
Recently, the development of brain functions, the cognitive capabilities of adolescents, and the effect of alcohol abuse on brain maturation have been examined. Adolescence is the time during which most individuals first experience alcohol exposure, and binge drinking is very common during this period.
Adolescence is a critical time period when cognitive, emotional, and social maturation occurs and it is likely that ethanol exposure may affect these complex processes. During a period that corresponds to adolescence in rats, the relatively brief exposure to high levels of alcohol via ethanol vapors caused long-lasting changes in functional brain activity.
Sex differences in many behaviors, including drug abuse, have been attributed to social and cultural factors. A male predominance in overall drug abuse appears by the end of adolescence, while girls develop a rapid progression from the time of the first abuse to dependence, and this represents female-based vulnerability. Recent studies have emphasized the contribution of sex differences in the function of the ascending DAergic systems, which are critical in reinforcement.
In addition, these studies have presented novel findings about the emergence of sex differences in DAergic function during adolescence. Increases in pubertal hormones, including gonadal and stress hormones, are a prominent developmental feature of adolescence and could contribute to the progression of sex differences in alcohol drinking behavior during puberty.
Witt 46 reviewed experimental and correlational studies of gonadal and stress-related hormone changes, as well as their effects on alcohol consumption and the associated neurobehavioral actions of alcohol on the mesolimbic dopaminergic system.
A major concern in this issue is recognizing the radiologic features of these CNS complications. Radiologists are supposed to be familiar with the early and late effects of cancer therapy in the pediatric CNS toxic effects, infection, endocrine or sensory dysfunction, neuropsychological impairment, and secondary malignancies in order to provide an accurate diagnosis and to minimize morbidity.
The acquisition of further knowledge about these complications will enable the development of more appropriate therapeutic decisions, effective patient surveillance, and an improved quality of life by decreasing the long-term consequences in survivors.
Certain chemotherapeutic compounds and environmental agents, such as anesthetics, antiepileptics, sleep-inducing and anxiolytic compounds, nicotine, alcohol, and stress, as well as agents of infection have also been investigated quite extensively and have been shown to contribute to the etiopathogenesis of serious neuropsychiatric disorders.
Several of these agents have contributed to the structural and functional brain abnormalities that have been observed in the biomarker profiles of schizophrenia and fetal alcohol syndrome.
The effects of these agents are generally permanent and irreversible. The rapid expansion of knowledge in this field, from basic science to clinical and community-based research, is expected to lead to urgently needed research in support of effective, evidence-based medicine and treatment strategies for undernutrition, overnutrition, and eating disorders in early childhood.
Eating is necessary for survival and provides a sense of pleasure, but may be perturbed, leading to undernutrition, overnutrition, and eating disorders. Furthermore, parenting, social factors, and food influence the development of eating behavior. Recently, the neural development of eating behavior in children has been investigated.
The range of exogenous agents, such as alcohol and cocaine, which are generally likely to detrimentally affect the development of the brain and CNS defies estimation, although the accumulated evidence is substantial. It has been postulated that, with adequate fish oils and fatty acids, the risk of psychopathology can be minimized, whereas a deficiency could lead to subcortical dysfunction in early puberty, and a breakdown of cortical circuitry and cognitive dysfunctions in late puberty.
The beneficial effect of fish oils and fatty acids in schizophrenia, fetal alcohol syndrome, developmental dyslexia, attention deficit hyperactivity disorder, and in other CNS disorders supports the hypothesis that the typical diet might be persistently deficient in the affected individuals, as illustrated in Figure 6.
However, the amount of fish oils and fatty acids needed to secure normal brain development and function is not known. It seems conjectural to postulate that a dietary deficiency in fish oils and fatty acids is causing brain dysfunction and death; however, all of these observations tend to suggest that a diet focusing on mainly protein is deficient, and the deficiency is most pronounced in maternal nutrition and in infancy, which might have a deleterious impact on the maturation of the adolescent brain.
Notes: MRI studies have provided evidence that in addition to the prefrontal cortex and limbic system, myelinogenesis and neurocircuitry remains under construction during adolescence.
Hence, consuming seafood may accelerate brain maturation in adolescents. However, malnutrition and substance abuse may inhibit maturation of the adolescent brain. Neuromorphological, neurochemical, neurophysiological, neurobehavioral, and neuropharmacological evidence suggests that the brain remains in its active state of maturation during adolescence. Computed tomography and MRI studies also provide evidence in support of this hypothesis. Brain maturation occurs during adolescence due to a surge in the synthesis of sex hormones implicated in puberty including estrogen, progesterone, and testosterone.
These sex hormones augment myelinogenesis and the development of the neurocircuitry involved in efficient neurocybernetics. Although tubulinogenesis, axonogenesis, and synaptogenesis can occur during the prenatal and early postnatal periods, myelinogenesis involved in the insulation of axons remains under construction in adolescence.
Sex hormones also significantly influence food intake and sleep requirements during puberty. In addition to dramatic changes in secondary sex characteristics, sex hormones may also influence the learning, intelligence, memory, and behavior of adolescents. Furthermore, it can be observed that the development of excitatory glutamatergic neurotransmission occurs earlier in the developing brain as compared to GABAergic neurotransmission, which makes the pediatric population susceptible to seizures.
The development and maturation of the prefrontal cortex occurs primarily during adolescence and is fully accomplished at the age of 25 years.
The development of the prefrontal cortex is very important for complex behavioral performance, as this region of the brain helps accomplish executive brain functions. A detailed study is required in order to determine the exact biomarkers involved, as well as the intricate influence of diet, drugs, sex, and sleep on the maturation of the adolescent brain as discussed briefly in this report.
The moral support and encouragement of President Kallol Guha is gratefully acknowledged. National Center for Biotechnology Information , U.
Journal List Neuropsychiatr Dis Treat v. Neuropsychiatr Dis Treat. Published online Apr 3. Author information Copyright and License information Disclaimer. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Adolescence is the developmental epoch during which children become adults — intellectually, physically, hormonally, and socially. Keywords: myelinogenesis, neurocircuitry, molecular imaging, drug addiction, behavior, social adjustment. Video abstract Click here to view. Open in a separate window. Figure 1. Factors influencing adolescent brain maturation. Figure 2. A diagram illustrating various stages of human brain development.
The adolescent brain It is well established that various morphological and physiological changes occur in the human brain during adolescence. Behavioral problems and puberty It is now known that hormones are not the only explanation for erratic adolescent behavior; hence, investigators are now trying to establish the exact nature of the interrelationship between pubertal processes and adolescent brain maturation. Figure 3. Prefrontal cortex Recently, investigators have studied various aspects of the maturation process of the prefrontal cortex of adolescents.
Figure 4. Risk-taking behavior The exact biological basis of risk-taking behavior in adolescents remains enigmatic. Figure 5. Leading cause of death among adolescents 10—24 years. How does setting affect theme? How does Diotima describe love?
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How do you address a shame in therapy? Why is it called present? Can you watch perseverance land? To elucidate the role LAMP in the establishment of cortical connections, we analyzed the outgrowth of thalamic and cortical explants prepared from presumptive limbic and non-limbic regions on membrane substrates of either LAMP-expressing CHO cells or on membranes of non-transfected CHO cells control. We found that length and sprouting of limbic thalamic and limbic cortical axons was enhanced on the LAMP substrate.
Non-limbic thalamic fibers, however, responded by exhibiting reduce outgrowth compared to control. The length and branching behavior of neocortical fibers was not affected by LAMP. In a second set of experiments, explants were cultured on native postnatal membranes prepared from limbic or neocortical areas.
Limbic thalamic and limbic cortical axons branched significantly more on membranes from limbic cortex, their target membranes, than on neocortical membranes. In contrast, non-limbic thalamic axons emitted more collaterals on membranes of neocortex. These branching preferences could be abolished by blocking LAMP on the membranes with a monoclonal antibody. Our results indicate that LAMP contributes to target recognition during cortical development through both attractive and repulsive mechanisms.
Moreover, these experiments suggest the existence of membrane-bound molecules that specify neocortical areas as target for appropriate thalamic and cortical afferents. Topographic projection is a general feature of brain architecture and is critical for appropriate information processing and coding. Nevertheless, little is known about the mechanisms that govern topographic organization.
Among the many regions exhibiting topographic relations, the limbic system has been the focus of intense interest, since it plays key roles in learning, memory, and motivated behavior. The Eph family receptor tyrosine kinases and ligands have been recently implicated in the specification of topographic maps. We have shown that Eph family receptors and ligands are expressed in complementary fashion in neurons and targets, respectively, in several regions of the limbic system.
For example, in the hippocampus, the Eph receptor Bsk is expressed in an increasing lateral to medial gradient. However, the spatial and temporal distribution of the ligands are different such that combinatorially they form a smooth dosromedial to ventrolateral gradient in the lateral septum, specifying the full target region during development.
Consistent with a key role in hippocamposeptal topographic projection, the ligands selectively inhibit the growth of the topographically inappropriate medial hippocampal neurites but sustain the growth of correct lateral neurites. Our studies indicate that the inhibitive interaction of Bsk and its ligands restrict the receptor-positive medial neurons to the topographically appropriate, ligand-poor dorsal septal target.
In addition to the hippocamposeptal system, BSK and its ligands are also expressed in afferents and targets of neurons from several other regions of the limbic system, including neurons in the mesolimbic pathway, which arises from the ventral tegmental dopaminergic neurons and terminates in the nucleus accumbens and limbic regions such as the amygdala. These observations indicate that the Eph family molecules play important roles in establishing the limbic neural circuits.
The formation of unique areas of the cerebral cortex during development is prerequisite for functional specialization. We have extended our earlier transplant studies to show that progenitor cells are particularly sensitive to environmental signals that control areal fate determination. Using expression of the limbic system-associated membrane protein LAMP as an assay for limbic phenotype, we have shown that progenitors isolated from different domains of presumptive neocortex and grown in culture can respond to LAMP-inducing signals.
Members of the epidermal growth factor receptor family, including those responsive to TGF and heregulin, can mediate cell fate decisions that occur independent of effects on proliferation or survival.
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