When do frontal lobes develop

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. Risk perception 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.

Self-regulation Self-regulation has been broadly classified as the management of emotions and motivation. Societal influences Mass media, community, and adult role models can also influence adolescent risk-taking behaviors.

Substance abuse The mechanisms underlying the long-term effects of prenatal substance abuse and its consequent elevated impulsivity during adolescence are poorly understood. Cannabis 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.

Nicotine 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.

Alcohol Recently, the development of brain functions, the cognitive capabilities of adolescents, and the effect of alcohol abuse on brain maturation have been examined. Sex differences Sex differences in many behaviors, including drug abuse, have been attributed to social and cultural factors. Nutrition 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.

Figure 6. Effect of seafood on the maturation of the adolescent brain. Conclusion Neuromorphological, neurochemical, neurophysiological, neurobehavioral, and neuropharmacological evidence suggests that the brain remains in its active state of maturation during adolescence.

Acknowledgments The moral support and encouragement of President Kallol Guha is gratefully acknowledged. Footnotes Disclosure The authors report no conflicts of interest in this report. References 1. Brain development during childhood and adolescence: a longitudinal MRI study. Nat Neurosci. Li K, Xu E.

The role and the mechanism of gamma-aminobutyric acid during central nervous system development. Neurosci Bull. Developmental changes in dopamine neurotransmission in adolescence: behavioral implications and issues in assessment. Brain Cogn. Kaplan PS. Sylwester R. The Adolescent Brain: Reaching for Autonomy.

Functional magnetic resonance imaging of facial affect recognition in children and adolescents. Dahl RE. Beyond raging hormones: the tinderbox in the teenage brain. Blakemore SJ. Development of the social brain in adolescence. J R Soc Med. The neural basis of puberty and adolescence. Sex steroids and connectivity in the human brain: a review of neuroimaging studies. Social cognitive development during adolescence. Soc Cogn Affect Neurosci. Doctoral Research Thesis. Amsterdam: The neurocognitive development of social decision making; pp.

McClure-Tone E. Behavioral and neural representation of emotional facial expressions across the lifespan. Dev Neuropsychol. Theories of adolescent risk taking The biopsychological model. In: Diclemente R. J, Santelli J. Adolescent egocentrism refers to: the thinking that leads young people to focus on themselves, and see what they do as the center of attention.

In fact, recent research has found that adult and teen brains work differently. Teens process information with the amygdala. What aspect of brain development might help to explain why a teenager can usually perform better as a babysitter than someone ten or eleven years old?

The prefrontal cortex helps the teen react in a more mature way than a 10 or 11 year old would. Under most laws, young people are recognized as adults at age This is due to falling levels of the chemicals that relay messages between your brain cells. Your brain is now also shrinking about 2 per cent every decade, as cells die in the prefrontal cortex, an area important for forming new memories and learning.

Developing physically into an adult takes 2 to 5 years. Most boys will stop growing taller by age 16 and will usually have developed fully by Since it controls vital functions such as breathing, swallowing, digestion, eye movement and heartbeat, there can be no life without it. But the rest of the brain is obviously capable of some remarkable feats, with one part able to compensate for deficiencies in another.

But it is not a final threshold. Doctors have long believed that if someone is without a heartbeat for longer than about 20 minutes, the brain usually suffers irreparable damage. When Is an Adolescent an Adult? Psychological Science, 27 4 , — Fair, D. Hartshorne, J.

When does cognitive functioning peak? The asynchronous rise and fall of different cognitive abilities across the life span. Psychological Science, 26 4 , — Hedman, A. Human brain changes across the life span: a review of 56 longitudinal magnetic resonance imaging studies. Human Brain Mapping, 33 8 , — Somerville, L. Neuron, 92 6 , — Sowell, E. Mapping cortical change across the human life span. Nature Neuroscience, 6 3 , — See how discoveries in the lab have improved human health.

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