Introduction

Exploring boundaries and displaying risk-taking behavior are part of adolescence. Many adolescents will display antisocial behavior (such as aggression, rule-breaking, delinquency, and other types of conduct that violate the basic rights of another person) at some point, usually limited to a single minor incident or offense. However, some adolescents display a persistent, pervasive pattern of antisocial behavior that is often already present in early adolescence or even childhood. Many of these persistent antisocial adolescents that habitually violate the rights of others and will not conform their behavior to the law or social norms are diagnosed with a conduct disorder (CD). Moreover, it has been shown that the most severe and persistent forms of CD include the presence of psychopathic traits in specific callous-unemotional (CU) traits. CU traits are characterized by lack of empathy, guilt or remorse, and a shallow or deficient affect, which are fairly stable until adulthood. In order to develop effective interventions to prevent the persistence of antisocial behavior and associated mental health problems, it is of main importance to gain more insight into the specific mechanisms involved in the development of this most severe type of antisocial behavior in youth.

Antisocial behavior is generally seen as a neurodevelopmental problem resulting from an interplay between neurobiological deficits, psychological and cognitive problems, and social adversity. This is reflected in the current biopsychosocial model for the development of antisocial behavior (see Figure 1). Based on this model, Popma and Raine (2006) already suggested that neurobiology should have a prominent part in the assessment and treatment of antisocial behavior [9]. Moreover, neurobiology may provide more insight into the different subtypes of antisocial behavior. According to the neurobiological model of Blair, impulsive antisocial behavior is thought to be related to reactive aggression and impaired decision making, mainly reflecting impairments in prefrontal functioning, while the more severe and persistent form of antisocial behavior with CU traits is related to intentional/proactive aggression and reduced responses to distress and unemotionality, reflecting reduced amygdala functioning. However, in spite of an enormous increase in research on neurobiological correlates of antisocial behavior since then, current youth forensic assessment and interventions still mainly focus on psychological, social, and environmental risks and protective factors.

Therefore, the aim of the current review is to give an overview of the current knowledge on the neurobiology of antisocial behavior in adolescents and to discuss how this knowledge can be translated to youth forensic clinical practice.

Neurobiology Of Antisocial Behavior

Genetics

There is a wealth of heritability studies that have analyzed empirical estimates of the relative contributions of genes and environment to the development of antisocial behavior. Recent analyses show that persistent delinquency has a substantial genetic origin (heritability 67%), aggressive behavior has a moderate heritability (39–46%), while conduct disorder in adolescence is about 50% genetic.

Specific genes have been associated with antisocial behavior (mainly dopaminergic, serotonergic, and oxytocin related), specifically in those with a history of child maltreatment. However, a meta-analysis of Genome-Wide Association Study (GWAS) data did not indicate robust and reproducible genetic variants associated with antisocial behavior. Antisocial behavior is most likely determined by many different genes, all of which have, at best, modest predictive value and are highly influenced by the heterogeneity of the phenotype of antisocial behavior and environmental influences. One of the new approaches to overcome this problem is the study of polygenic risk score (PRS), a technique to estimate the effect of many genetic variants together on a specific phenotype or behavioral characteristic. Indeed, recent analyses show that polygenic risk score explained the differences between stable low and high aggressive behavior throughout adolescence, as well as confirmed involvement of glutamatergic, dopaminergic, and neuroendocrine genetic variation in aggression and CU-traits, explaining up to 2% of explained variance in uncaring and unemotional behavior.

Neuroimaging

Structural and functional magnetic resonance imaging (MRI) studies have resulted in a wealth of knowledge on brain development during adolescence, showing that (part of) the normative peak in risk behaviors that many typical-developing adolescents display can be explained by a relative protracted development of frontal cortical cognitive control systems, combined with fast maturity of subcortical socio-affective systems. As stated above, for most youths, this behavior is incidental and limited to adolescence. However, studies in adolescents with severe and persistent antisocial behavior, including those with CD and/or CU traits, showed specific structural and functional deficits in brain development, mainly in prefrontal and subcortical (para)limbic areas and the connectivity between those areas.

First, structural brain alterations in (familial risk for) CD include smaller volumes of the frontal lobe, superior temporal gyrus, (inferior) parietal lobe, and occipital lobe, as well as smaller cingulate cortex volumes. In addition, some evidence is found for specific structural gray matter alterations in frontal and limbic regions related to a history of childhood maltreatment in CD. Although minimal evidence for structural abnormalities was found for CU-traits, some studies show specific structural and functional abnormalities in limbic and paralimbic structures. As for structural connections, i.e., white matter tracts, aggression has been related to diminished white matter density in pathways connecting subcortical and cortical regions, while CD and specifically CU traits have been related to alterations in additional, key subcortical-cortical and cortico-cortical connections (e.g., cingulum in CD males; CU-traits: corpus callosum, anterior thalamic radiation, uncinate fasciculus.

With respect to functional MRI, severe antisocial behavior has also been related to aberrant subcortical socio-emotional activation. This is reflected in differences in reward-related striatum and orbitofrontal cortex (OFC) functioning compared to the typical developing youth and alterations in amygdala activity related to the processing of emotional faces, empathy, and threat acquisition, particularly in youth with high CU traits. Finally, studies on functional connectivity, i.e., resting-state brain activity, suggest that CD is characterized by aberrant connectivity mainly in default mode, sensorimotor networks, and limbic system. Moreover, proactive aggression and CU traits were related to specific connectivity patterns involving areas associated with emotion, empathy, morality, and cognitive control. (e.g. amygdala-precuneus coupling, frontal, parietal, and cingulate areas).

Neuropsychology

Overall, offending youth show impairments in neurocognitive functioning. Adolescents who show antisocial and psychopathic behaviors tend to have lower IQs; specifically, low verbal IQs, have been found.

As for specific neuropsychological deficits, altered patterns of cognitive functioning in antisocial behavior largely overlap with deficits in structural and functional brain abnormalities in prefrontal and subcortical limbic structures. The most empirical support refers to the existence of problems or deficits in Executive Functioning (EF). Executive functioning is an umbrella term for mental top-down brain processes necessary to adapt behaviors to novel situations. Deficits in executive functions such as response inhibition, working memory, and mental flexibility have been found in CD and in psychopathic traits in young adults. Dysfunctions in EF may also be the mediating factor between traumatic brain injury and antisocial behavior. Executive functions such as (social attention, cognitive flexibility, working memory, and social planning) are also the basis of many emotional and social skills. At the level of emotion processing, specific deficits in emotion recognition, emotional learning, and emotion regulation have been found in youth with CD, which may be related to CU traits. However, another study found no specific relation with CU traits in CD.

Neurophysiology and neuroendocrinology

The autonomic nervous system (ANS) is among the most studied systems in antisocial behavior. According to the low-arousal theory, antisocial behavior is related to a low ANS activity, which subsequently may lead to sensation-seeking behavior, as well as fearlessness. An extensive meta-analysis showed that low resting heart rate is the most stable correlate of antisocial behavior throughout adolescence and early adulthood, with the strongest effects among the more serious antisocial groups, such as serious offenders and subjects with psychopathic traits. However, not all studies could replicate this finding. This is most likely due to heterogeneity within CD, as adolescents with high CU traits and proactive aggressive behavior have low arousal levels, while adolescents with more anxiety and reactive aggressive behavior show high arousal levels.

As for ANS reactivity, Respiratory Sinus Arrhythmia (RSA) has been most extensively studied as an indicator of emotion regulation. Several studies show a decreased RSA responsivity in reaction to diverse emotional stimuli, although results are less consistent than for resting heart rate.

Several studies have specifically focused on stress reactivity in antisocial behavior, mostly including heart rate and/or the so-called stress hormone cortisol. These studies also showed a decreased responsivity in adolescents with antisocial disorders, with the main effects in those with CU traits. Furthermore, dorsal striatum activity as part of the mesolimbic system, known to be sensitive to environmental adversity, seems to play a role in externalization-specific cortisol stress responses. However, a recent review on the association of basal and reactivity cortisol levels with the development of delinquent behavior did show inconsistent results.

Finally, sex hormones, specifically testosterone in males, have been related to aggressive behavior and CD.

A recent multisample, multimethod study of our own group has integrated neurophysiological and neuroendocrinological assessments over several antisocial and normal developing cohorts. This large study confirms the importance of both neurophysiology and neuroendocrinology: both are related to antisocial behavior, such as psychopathic traits, and aggressive and impulsive behavior; moreover, these relations showed to be consistent throughout adolescence and early adult hood.

Translation Of Neurobiological Knowledge To Youth Forensic Clinical Practice

Diagnostics and risk taxation

Based on the current knowledge described above, using neurobiological knowledge to make a distinction between antisocial behavior with or without psychopathic traits and CU traits, in specific, may be most valuable for clinical forensic practice. Neurobiological assessments may provide additional indicators of CU traits that are more objective than self-report only. Based on the current literature, the most promising and practical assessments to differentiate between antisocial youth with or without CU traits are neurophysiological (heart rate, heart rate variability/RSA) and neuroendocrinological (cortisol, testosterone) measures that are related to stress and emotion processing, as well as neuropsychological functions such emotion recognition, emotional learning, and emotion regulation, which are also related to structural and functional deficits in subcortical limbic structures such as the amygdala in antisocial youth with CU traits. Assessment of executive functioning, which is the basis of many emotional and social skills, is also relevant in this respect.

Moreover, in line with the biopsychosocial model, it is important to stress that neurobiological assessments should be integrated with psychosocial assessments, as several studies have found an association between parental antisocial behavior, harsh parenting, and maltreatment and lower heart rate and altered basal RSA levels in antisocial youth with our without CU traits. This may indicate potential physiological pathways through which genetics and child maltreatment may impact the development of antisocial behavior and CU traits, as was also posed in Blair’s neurobiological model of the development of psychopathic traits.

Finally, as for risk taxation, recent studies by our own groups have shown significant additional value of neurophysiological and neuroendocrinological measures to standard psychosocial risk assessment for the prediction of (violent) reoffending in severe antisocial and delinquent youth.

Treatment and treatment evaluation

Currently, the main challenge lies in translating neurobiological knowledge into effective interventions for antisocial youth.

First, neurobiological knowledge is important for the psychoeducation of youth and parents. Increasing their knowledge regarding the neurobiological processes that underlie the development may help youth to better understand their behavior. It should, however, be stressed that, although antisocial behavior has a relatively high heritability, which is related to deficits in brain development and functioning, current knowledge does not support the idea that people are ‘determined by their brains to commit crimes’. A 50–60% heritability still leaves a large contribution to the environment. Moreover, specifically during adolescence, the brain is still in development and flexible, which forms a window of opportunity for interventions to steer away from further antisocial development.

Second, neurobiological findings may guide specific interventions to change the developmental trajectory of antisocial behaviors. For severe delinquent youth, neurobiological insights on antisocial development may help to promote effective interventions within the juvenile justice system.

As for specific neurobiologically informed interventions, pharmacologic interventions that target dopaminergic, noradrenergic, and serotonergic activity, including psychostimulants, alpha-2 agonists, atomoxetine, and risperidone, -have shown benefits. Specifically for methylphenidate, functional brain imaging studies show that methylphenidate may normalize subcortical, specifically amygdala functioning, as well as resting-state functional connectivity of mesolimbic seed regions with areas involved in moral decision making, visual processing, and attention in adolescents with conduct disorder that have been related to antisocial behavior and CU traits.

However, neurobiologically informed interventions do not necessarily have to involve interventions at the pharmacological level. Interventions aimed at improving the neuropsychological functioning of antisocial youth, such as cognitive training and improving cognitive control, have also been found to be promising. Specific training in executive functioning in combination with parental training in perseverance may reduce proactive aggression. Recently, a specific intervention program for high-risk children, based on individual neuropsychological profiles, has been shown to be effective in reducing antisocial behavior.

As for aggression and emotion regulation, it has been shown that aggression may be reduced by changing self-control using Triple P, Aggression Replacement Therapy (ART) etc.; moreover, ART has also been shown to be able to actually normalize neuroendocrine functioning, also in antisocial youth with CU traits.

Finally, at the neurophysiological level, a promising approach may be biofeedback using wearables to improve awareness of physiological signals preceding aggressive outbursts and stimulate emotion and aggression regulation.

Translational Research Agenda

Although, as we have seen above, there is ample knowledge available on the neurobiology of antisocial behavior, and some promising neurobiologically informed interventions have already been tested, there are some gaps in knowledge that hamper full translation to clinical practice.

First, we need more knowledge on the interplay between neurobiological, psychological, and biological characteristics. Current neurobiological research has mainly focused on one or two neurobiological factors, and in some cases, on the interaction with one or two environmental factors; however, from a biopsychosocial perspective, it is of main importance to integrate neurobiological assessments with the mainly psychosocial assessments that are currently used in clinical practice. Our previous work has shown that such an approach does have enormous power in improving the prediction of reoffending; moreover, this may also provide more insight in the underlying mechanisms involved in the different subtypes of antisocial behavior, such as the group with severe and persistent antisocial behavior that also display CU traits.

Second, most findings are on the group level and therefore difficult to translate to interventions at the individual level. Through structural biopsychosocial assessments in clinical practice, longitudinal data will become available that can be used to create open-source models and algorithms that can be utilized to predict individual treatment outcomes.

Third, although there are some indications that interventions do change neurobiological characteristics, we need more knowledge on the changeability of neurodevelopmental and neurobiological characteristics of antisocial youth in response to treatment. This fundamental knowledge is essential to determine whether there is still enough neuroplasticity to steer an initial antisocial development in a positive direction.

In conclusion, this review has shown that there is a wealth of knowledge available already on the genetic, neuroimaging, neuropsychological, neurophysiological, and neuroendocrinological correlates of antisocial behavior in adolescents; however, it also shows that, in order to move the field forward and create direct clinical relevance, the main goal of future neurobiological research in antisocial behavior should be to better integrate neurobiological research in clinical practice in order to study individual biopsychosocial profiles and the changeability thereof in relation to treatment. To achieve this goal, we need a translational, iterative approach in which we not only observe but also intervene in clinical practice in collaboration with clinical partners. Together, we have to engage in a translational research cycle consisting of consolidation of (existing) knowledge; translation of knowledge in integrated assessments, interventions, and education; implementation of integrated knowledge; monitoring of the use of this knowledge; and evaluation of validity, usability, and affectivity. Importantly, this cycle is dynamic, meaning that fundamental knowledge is constantly updated, and information flows both toward as well as back from clinical practice (Figure 2). Eventually, this will help us to translate fundamental neurobiological research into personalized treatment programs that are based on the individual biopsychosocial profiles of antisocial youth.

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Introduction

Adolescence is a period characterized by exploration and risk-taking, with many youths engaging in some degree of antisocial behavior (e.g., aggression, rule-breaking). While typically transient, a subset of adolescents exhibit persistent, pervasive antisocial behavior, often beginning in early adolescence or childhood. These individuals, frequently diagnosed with conduct disorder (CD), persistently violate societal norms and the rights of others. A particularly severe form of CD involves the presence of callous-unemotional (CU) traits, marked by a lack of empathy, guilt, and remorse, and shallow affect, often persisting into adulthood. Understanding the mechanisms driving this severe form of antisocial behavior is crucial for developing effective interventions.

Antisocial behavior is understood as a neurodevelopmental issue arising from an interplay of neurobiological deficits, psychological and cognitive challenges, and social adversity, as encapsulated in the biopsychosocial model. This model underscores the significance of neurobiological factors in the assessment and treatment of antisocial behavior, potentially elucidating different subtypes. For instance, Blair's neurobiological model posits that impulsive antisocial behavior, linked to reactive aggression and impaired decision-making, primarily reflects prefrontal dysfunction. Conversely, severe, persistent antisocial behavior with CU traits, associated with proactive aggression and diminished responsiveness to distress, implicates reduced amygdala functioning. Despite substantial advancements in neurobiological research, current youth forensic assessments and interventions remain largely centered on psychosocial factors.

This review aims to synthesize the existing knowledge base on the neurobiology of antisocial behavior in adolescents and explore its potential applications in youth forensic clinical practice.

Neurobiology of Antisocial Behavior

Genetics

Extensive heritability studies have estimated the relative genetic and environmental contributions to antisocial behavior. Persistent delinquency demonstrates a substantial genetic component (67% heritability), while aggressive behavior shows moderate heritability (39–46%). Conduct disorder in adolescence exhibits approximately 50% heritability.

Research has identified associations between specific genes (primarily those related to dopaminergic, serotonergic, and oxytocin systems) and antisocial behavior, particularly in individuals with a history of child maltreatment. However, robust and replicable genetic variants associated with antisocial behavior have yet to be identified through genome-wide association studies (GWAS). The complex etiology of antisocial behavior likely involves multiple genes with modest predictive power, further influenced by phenotypic heterogeneity and environmental factors. Polygenic risk score (PRS) analysis, a technique for evaluating the collective impact of multiple genetic variants, has emerged as a promising approach. Recent studies using PRS have found that it accounts for differences in stable aggressive behavior during adolescence and supports the role of glutamatergic, dopaminergic, and neuroendocrine genetic variations in aggression and CU traits.

Neuroimaging

Structural and functional magnetic resonance imaging (MRI) studies have yielded significant insights into adolescent brain development. The normative surge in risk-taking observed in typically developing adolescents can be partly attributed to the asynchronous development of frontal cortical cognitive control systems and the rapid maturation of subcortical socio-affective systems. In contrast, adolescents with severe and persistent antisocial behavior, including those with CD and/or CU traits, display distinct structural and functional deficits, primarily in prefrontal, subcortical (para)limbic areas, and their interconnectivity.

Structural brain abnormalities in (individuals at familial risk for) CD include reduced volumes in the frontal lobe, superior temporal gyrus, (inferior) parietal lobe, occipital lobe, and cingulate cortex. Additionally, some studies suggest specific structural gray matter alterations in frontal and limbic regions associated with childhood maltreatment in CD. While evidence for structural abnormalities in CU traits is limited, some studies report specific structural and functional differences in limbic and paralimbic structures. Regarding white matter tracts, aggression is linked to reduced white matter density in pathways connecting subcortical and cortical regions. CD and CU traits, in particular, are associated with alterations in crucial subcortical-cortical and cortico-cortical connections.

Functional MRI studies reveal aberrant subcortical socio-emotional activation in severe antisocial behavior, manifested as differences in reward-related striatum and orbitofrontal cortex (OFC) functioning compared to typically developing youth. Additionally, alterations in amygdala activity during emotional face processing, empathy, and threat acquisition are observed, particularly in youth with prominent CU traits. Resting-state functional connectivity studies suggest that CD is characterized by abnormal connectivity primarily in the default mode, sensorimotor, and limbic networks. Proactive aggression and CU traits are associated with specific connectivity patterns involving areas linked to emotion, empathy, morality, and cognitive control.

Neuropsychology

Offending youth generally exhibit impairments in neurocognitive functioning, with adolescents exhibiting antisocial and psychopathic traits often demonstrating lower IQ scores, particularly in the verbal domain.

Neuropsychological deficits in antisocial behavior largely mirror the structural and functional brain abnormalities observed in prefrontal and subcortical limbic structures. Deficits in executive functions (EF), including response inhibition, working memory, and mental flexibility, are well-documented in both CD and psychopathic traits in young adults. EF dysfunction may mediate the relationship between traumatic brain injury and antisocial behavior. Furthermore, EF, encompassing social attention, cognitive flexibility, working memory, and social planning, underpins numerous emotional and social skills. In terms of emotion processing, specific deficits in emotion recognition, emotional learning, and emotion regulation are found in youth with CD, potentially related to CU traits, although findings regarding the relationship with CU traits are inconsistent.

Neurophysiology and Neuroendocrinology

The autonomic nervous system (ANS) has been extensively studied in the context of antisocial behavior. The low-arousal theory posits that low ANS activity contributes to sensation-seeking and fearlessness in antisocial individuals. Meta-analytic evidence supports low resting heart rate as a stable correlate of antisocial behavior throughout adolescence and early adulthood, with the strongest effects observed in severe antisocial groups (e.g., serious offenders, individuals with psychopathic traits). However, this finding is not universally consistent, likely due to heterogeneity within CD. Adolescents with high CU traits and proactive aggression tend to exhibit low arousal levels, while those with higher anxiety and reactive aggression display high arousal levels.

Respiratory Sinus Arrhythmia (RSA), an indicator of emotion regulation, has been extensively studied as a measure of ANS reactivity. Several studies report decreased RSA responsivity to emotional stimuli in antisocial youth, although findings are less consistent compared to resting heart rate.

Stress reactivity research, often focusing on heart rate and cortisol (the "stress hormone"), has also revealed decreased responsivity in adolescents with antisocial disorders, particularly those with CU traits. Dorsal striatum activity, part of the mesolimbic system and sensitive to environmental adversity, appears to be involved in externalizing-specific cortisol stress responses. However, a recent review found inconsistent results regarding the association between basal and reactivity cortisol levels and delinquent behavior.

Lastly, sex hormones, specifically testosterone in males, have been linked to aggressive behavior and CD.

A recent multisample, multimethod study provided further support for the role of neurophysiology and neuroendocrinology in antisocial behavior. The study demonstrated consistent relationships between these factors and antisocial traits, aggressive behavior, and impulsive behavior across adolescence and early adulthood.

Translation of Neurobiological Knowledge to Youth Forensic Clinical Practice

Diagnostics and Risk Assessment

Current neurobiological knowledge holds particular promise for differentiating between antisocial behavior with and without psychopathic traits, specifically CU traits, in clinical forensic settings. Neurobiological assessments can offer more objective indicators of CU traits compared to self-report measures alone. Based on existing literature, the most promising and feasible assessments for this purpose are neurophysiological (heart rate, heart rate variability/RSA) and neuroendocrinological (cortisol, testosterone) measures related to stress and emotion processing. Neuropsychological assessments of emotion recognition, emotional learning, emotion regulation, and executive functioning are also relevant, as these functions are often impaired in antisocial youth with CU traits.

It is essential to emphasize that neurobiological assessments should be integrated with psychosocial evaluations, as research has established a link between parental antisocial behavior, harsh parenting, maltreatment, and lower heart rate and altered basal RSA levels in antisocial youth, both with and without CU traits. This suggests potential physiological pathways through which genetics and early adversity influence the development of antisocial behavior and CU traits, aligning with Blair's neurobiological model.

In terms of risk assessment, recent studies have demonstrated the added value of incorporating neurophysiological and neuroendocrinological measures into standard psychosocial risk assessments for predicting (violent) reoffending in severe antisocial and delinquent youth.

Treatment and Treatment Evaluation

Translating neurobiological knowledge into effective interventions for antisocial youth presents a significant challenge.

Firstly, neurobiological findings can inform psychoeducation for both youth and their parents. Enhancing their understanding of the neurobiological underpinnings of antisocial behavior can be empowering, particularly given the common misconception that individuals with such behavior are "hardwired" to offend. Despite the substantial heritability of antisocial behavior and its association with neurodevelopmental differences, it is crucial to emphasize that individuals are not predetermined to engage in criminal behavior. The brain remains malleable, particularly during adolescence, presenting a window of opportunity for interventions to alter antisocial trajectories.

Secondly, neurobiological insights can guide the development of interventions tailored to modify the developmental trajectory of antisocial behavior. Specifically, they can inform the design and implementation of effective interventions within the juvenile justice system.

Neurobiologically informed interventions can take various forms, including pharmacological and behavioral approaches. Pharmacologic interventions targeting dopaminergic, noradrenergic, and serotonergic activity have shown promise. For example, functional brain imaging studies suggest that methylphenidate may normalize subcortical (particularly amygdala) functioning and resting-state functional connectivity in adolescents with conduct disorder.

However, neurobiologically informed interventions are not limited to pharmacological approaches. Interventions targeting the neuropsychological functioning of antisocial youth, such as cognitive training programs aimed at improving cognitive control, have shown potential. Combining executive functioning training with parental training in perseverance can reduce proactive aggression. Recently, an individualized intervention program based on neuropsychological profiles has demonstrated effectiveness in reducing antisocial behavior in high-risk children.

For aggression and emotion regulation, interventions like Triple P and Aggression Replacement Therapy (ART) have shown efficacy in reducing aggression by enhancing self-control. Importantly, ART has demonstrated the ability to normalize neuroendocrine functioning, even in antisocial youth with CU traits.

At the neurophysiological level, biofeedback using wearables is a promising avenue for increasing awareness of physiological precursors to aggressive outbursts and promoting emotion regulation and aggression control.

Translational Research Agenda

Despite the considerable knowledge base on the neurobiology of antisocial behavior and the development of some promising neurobiologically informed interventions, several knowledge gaps hinder full translation to clinical practice.

Firstly, a more comprehensive understanding of the complex interplay between neurobiological, psychological, and social factors is needed. Most neurobiological research has focused on a limited number of factors in isolation. A holistic biopsychosocial perspective necessitates the integration of neurobiological assessments with existing psychosocial assessments used in clinical practice. This integrated approach has the potential to enhance reoffending prediction and provide a deeper understanding of the mechanisms driving different subtypes of antisocial behavior.

Secondly, translating group-level findings to individual-level interventions remains challenging. Longitudinal data from comprehensive biopsychosocial assessments in clinical practice can facilitate the development of open-source models and algorithms to predict individual treatment outcomes.

Thirdly, although some evidence suggests that interventions can modify neurobiological characteristics, further research is needed to understand the extent to which neurodevelopmental and neurobiological features of antisocial youth are amenable to change through treatment. This knowledge is crucial for determining the degree of neuroplasticity available for redirecting antisocial development.

In conclusion, while a substantial body of knowledge exists on the genetic, neuroimaging, neuropsychological, neurophysiological, and neuroendocrinological correlates of antisocial behavior in adolescents, bridging the gap between research and clinical practice is paramount. Future research should prioritize integrating neurobiological assessments into clinical practice to enable the study of individual biopsychosocial profiles and their responsiveness to treatment. This requires a collaborative, translational approach involving researchers and clinicians, engaging in a cyclical process of knowledge consolidation, translation, implementation, monitoring, and evaluation. This collaborative effort will pave the way for translating fundamental neurobiological research into personalized treatment programs tailored to the unique biopsychosocial profiles of antisocial youth.

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Introduction

During adolescence, it's normal for individuals to explore their boundaries and engage in some level of risk-taking. Many adolescents might display antisocial behaviors, such as aggression, breaking rules, delinquency, or other actions that infringe upon the rights of others. This behavior is often temporary and limited to minor incidents. However, some adolescents exhibit a persistent and widespread pattern of antisocial behavior that often emerges in early adolescence or even childhood. Many of these individuals, who consistently violate the rights of others and defy social norms and laws, are diagnosed with conduct disorder (CD). Research indicates that the most severe and persistent forms of CD often involve psychopathic traits, particularly callous-unemotional (CU) traits. These traits are characterized by a lack of empathy, guilt, remorse, and shallow emotions, which tend to remain stable into adulthood. To develop effective strategies for preventing the continuation of antisocial behavior and related mental health issues, it is crucial to gain a deeper understanding of the specific mechanisms driving the development of this severe form of antisocial behavior in young people.

Antisocial behavior is generally understood as a neurodevelopmental issue arising from a complex interplay of neurobiological deficits, psychological and cognitive challenges, and social adversity. This understanding is reflected in the current biopsychosocial model of antisocial behavior development. Based on this model, experts have suggested that neurobiology should play a central role in assessing and treating antisocial behavior. Additionally, neurobiology may provide further insights into the different subtypes of antisocial behavior. One prominent neurobiological model proposes that impulsive antisocial behavior is linked to reactive aggression and impaired decision-making, primarily reflecting problems in the prefrontal cortex. On the other hand, the more severe and enduring form of antisocial behavior with CU traits is associated with intentional/proactive aggression and diminished responses to distress and emotions, suggesting reduced amygdala activity. However, despite substantial growth in research on the neurobiological correlates of antisocial behavior, current assessments and interventions within youth forensic settings primarily focus on psychological, social, and environmental risk and protective factors.

This review aims to provide a comprehensive overview of the current understanding of the neurobiology of antisocial behavior in adolescents and to explore how this knowledge can be applied to youth forensic clinical practice.

The Neurobiology of Antisocial Behavior

Genetics

Numerous heritability studies have investigated the relative contributions of genes and environment to the development of antisocial behavior. Recent findings reveal that persistent delinquency has a strong genetic basis (67% heritability), aggressive behavior has a moderate heritability (39–46%), while conduct disorder in adolescence is approximately 50% genetic.

Specific genes, mainly related to dopamine, serotonin, and oxytocin, have been linked to antisocial behavior, particularly in individuals with a history of child maltreatment. However, a meta-analysis of genome-wide association studies (GWAS) did not identify any reliable and consistently replicated genetic variants directly associated with antisocial behavior. It's highly probable that antisocial behavior is influenced by a multitude of genes, each with a relatively small predictive value. These genes are also likely susceptible to the heterogeneity of antisocial behavior and environmental influences. A newer approach to address this complexity is the study of polygenic risk scores (PRS), a technique that estimates the combined effect of numerous genetic variants on a particular trait or behavior. Recent studies using PRS have shown that it can explain differences in stable low and high aggressive behavior throughout adolescence and confirm the involvement of genetic variations related to glutamate, dopamine, and neuroendocrine systems in aggression and CU traits.

Neuroimaging

Studies using structural and functional magnetic resonance imaging (MRI) have provided extensive knowledge about brain development during adolescence. These studies show that the typical increase in risk-taking behavior seen in many adolescents can be partially explained by the relatively slower development of the frontal cortex, responsible for cognitive control, compared to the faster maturation of subcortical regions involved in socio-emotional responses. For most young people, this behavior is temporary and specific to adolescence. However, studies on adolescents with severe and persistent antisocial behavior, including those with CD and/or CU traits, have identified specific structural and functional abnormalities in brain development, primarily in prefrontal and subcortical areas (especially limbic structures) and the connections between these regions.

Structural brain differences observed in individuals with (a family risk for) CD include reduced volumes of the frontal lobe, superior temporal gyrus, (inferior) parietal lobe, and occipital lobe, as well as smaller cingulate cortex volumes. Some evidence also suggests specific structural alterations in gray matter within frontal and limbic regions associated with a history of childhood maltreatment in CD. While evidence for structural abnormalities specific to CU traits is limited, some studies have reported unique structural and functional abnormalities in limbic and paralimbic structures. Regarding structural connections, meaning white matter tracts, aggression has been linked to reduced white matter density in pathways connecting subcortical and cortical areas. CD and, more specifically, CU traits have been associated with changes in crucial subcortical-cortical and cortico-cortical connections.

In terms of functional MRI, severe antisocial behavior has been linked to atypical activity in subcortical regions involved in processing social and emotional information. This is evident in differences in reward-related activity in the striatum and orbitofrontal cortex (OFC) compared to typically developing youth and alterations in amygdala activity during the processing of emotional faces, empathy, and threat learning, particularly in youth with high CU traits. Lastly, studies on functional connectivity, examining resting-state brain activity, indicate that CD is characterized by abnormal connectivity primarily in the default mode network, sensorimotor networks, and the limbic system. Proactive aggression and CU traits were linked to distinct connectivity patterns involving brain areas associated with emotion, empathy, morality, and cognitive control.

Neuropsychology

Generally, young people who engage in offending behavior exhibit impairments in neurocognitive functioning. Adolescents with antisocial and psychopathic behaviors tend to have lower IQ scores, particularly lower verbal IQs.

Concerning specific neuropsychological deficits, the altered patterns of cognitive functioning in antisocial behavior significantly overlap with the observed structural and functional brain abnormalities in prefrontal and subcortical limbic regions. The most robust evidence points to problems or deficits in executive functioning (EF), which refers to higher-level mental processes that allow us to adapt our behavior to new situations. Deficits in EF, such as response inhibition, working memory, and mental flexibility, have been observed in individuals with CD and in young adults with psychopathic traits. These EF impairments might also be the mediating factor between traumatic brain injury and antisocial behavior.

Executive functions (e.g., social attention, cognitive flexibility, working memory, and social planning) underpin many emotional and social skills. At the level of emotion processing, specific deficits in recognizing, learning from, and regulating emotions have been found in young people with CD, which may be associated with CU traits. However, it's worth noting that not all studies have found a direct link between these emotional processing deficits and CU traits in CD.

Neurophysiology and Neuroendocrinology

The autonomic nervous system (ANS) is one of the most extensively studied systems in relation to antisocial behavior. According to the low-arousal theory, antisocial behavior is connected to reduced ANS activity, which might subsequently lead to sensation-seeking behavior and fearlessness. A comprehensive meta-analysis showed that a low resting heart rate is the most consistent biological correlate of antisocial behavior throughout adolescence and early adulthood, with the strongest effects observed in individuals with more severe forms of antisocial behavior, such as serious offenders and those with psychopathic traits. However, it's important to acknowledge that not all studies have been able to replicate this finding. This inconsistency is likely due to the heterogeneity within CD, as individuals with high levels of CU traits and proactive aggression tend to exhibit low arousal, while those with more anxiety and reactive aggression display high arousal.

Regarding ANS reactivity, respiratory sinus arrhythmia (RSA) has been extensively studied as a physiological indicator of emotion regulation. A number of studies have reported decreased RSA reactivity in response to various emotional stimuli in antisocial youth, although the findings are less consistent compared to resting heart rate.

Several studies have specifically examined stress reactivity in antisocial behavior, primarily focusing on heart rate and/or the stress hormone cortisol. These studies have generally found a blunted stress response in adolescents with antisocial disorders, with the most pronounced effects in those with CU traits. Furthermore, activity in the dorsal striatum, a part of the mesolimbic system sensitive to environmental adversity, appears to be involved in externalizing-specific cortisol stress responses. It is important to note, however, that a recent review on the relationship between basal and reactive cortisol levels and delinquent behavior reported inconsistent findings.

Lastly, sex hormones, particularly testosterone in males, have been linked to aggressive behavior and CD.

A recent large-scale study that combined data from multiple samples and employed various methods to investigate neurophysiological and neuroendocrinological measures across several antisocial and typically developing cohorts confirmed the significance of both systems. The study found that both neurophysiology and neuroendocrinology are associated with antisocial behaviors, such as psychopathic traits, aggression, and impulsivity. Moreover, these relationships were found to be consistent across adolescence and early adulthood.

Applying Neurobiological Knowledge in Youth Forensic Clinical Practice

Diagnostics and Risk Assessment

Based on the current understanding, applying neurobiological knowledge to distinguish between antisocial behavior with or without psychopathic traits, and CU traits specifically, could be highly valuable in forensic clinical practice. Neurobiological assessments might provide additional, more objective indicators of CU traits compared to relying solely on self-report measures. Based on the existing literature, the most promising and practical assessments for differentiating between antisocial youth with or without CU traits are neurophysiological measures (heart rate, heart rate variability/RSA), neuroendocrinological measures (cortisol, testosterone), which are associated with stress and emotional processing, and neuropsychological assessments of functions like emotion recognition, emotional learning, and emotion regulation. These functions have been linked to structural and functional deficits in subcortical limbic structures, such as the amygdala, in antisocial youth with CU traits. Assessing executive functioning, which forms the basis for many emotional and social skills, is also relevant in this context.

Furthermore, in line with the biopsychosocial model, it is essential to emphasize that neurobiological assessments should be integrated with psychosocial assessments. Several studies have reported associations between parental antisocial behavior, harsh parenting, maltreatment, lower heart rate, and altered basal RSA levels in antisocial youth, both with and without CU traits. This suggests potential physiological pathways through which genetics and child maltreatment might influence the development of antisocial behavior and CU traits, as proposed in Blair’s neurobiological model of psychopathy development.

Finally, regarding risk assessment, recent studies have demonstrated the significant added value of incorporating neurophysiological and neuroendocrinological measures into standard psychosocial risk assessments for predicting (violent) reoffending in severely antisocial and delinquent youth.

Treatment and Treatment Evaluation

Currently, the main challenge lies in translating existing neurobiological knowledge into effective interventions for antisocial youth.

Firstly, neurobiological knowledge is crucial for educating both youth and their parents. Enhancing their understanding of the neurobiological processes underpinning this behavior may help young individuals better comprehend their own actions. However, it is crucial to emphasize that while antisocial behavior has a relatively strong genetic component, which is associated with deficits in brain development and function, current research does not support the notion that individuals are "predetermined by their brains to commit crimes." A heritability of 50–60% still leaves substantial room for environmental influences. Moreover, the brain remains highly malleable and adaptable, especially during adolescence, presenting a valuable window of opportunity for interventions to redirect antisocial development.

Secondly, neurobiological findings can guide the development of targeted interventions to alter the developmental trajectory of antisocial behaviors. For severely delinquent youth, neurobiological insights into antisocial development can be instrumental in promoting effective interventions within the juvenile justice system.

Regarding specific neurobiologically informed interventions, pharmacological treatments targeting dopamine, norepinephrine, and serotonin activity, such as psychostimulants, alpha-2 agonists, atomoxetine, and risperidone, have shown some benefits. For methylphenidate specifically, functional brain imaging studies suggest that it may normalize activity in subcortical regions, particularly the amygdala, as well as resting-state functional connectivity between mesolimbic seed regions and areas involved in moral decision-making, visual processing, and attention in adolescents with conduct disorder. These brain regions and networks have been implicated in antisocial behavior and CU traits.

However, neurobiologically informed interventions don't necessarily have to involve medications. Interventions aimed at enhancing the neuropsychological functioning of antisocial youth, such as cognitive training programs designed to improve cognitive control, have also shown promise. Specific training targeting executive functions, combined with parental training in encouraging perseverance, may reduce proactive aggression. Recent research has shown that an intervention program tailored to the specific neuropsychological profiles of high-risk children can effectively reduce antisocial behavior.

Regarding aggression and emotion regulation, studies have demonstrated that aggression can be reduced by teaching self-control strategies, such as those taught in programs like Triple P and Aggression Replacement Therapy (ART). Moreover, ART has also been found to normalize neuroendocrine functioning, even in antisocial youth with CU traits.

Finally, at the neurophysiological level, biofeedback using wearable technology is a promising approach. Biofeedback can help individuals become more aware of physiological signals that precede aggressive outbursts, promoting better emotion and aggression regulation.

Translational Research Agenda

While there is a substantial body of knowledge about the neurobiology of antisocial behavior and some promising neurobiologically informed interventions have been tested, several knowledge gaps hinder their full translation into clinical practice.

Firstly, further research is needed to understand the complex interplay between neurobiological, psychological, and social factors. Current neurobiological research has predominantly focused on one or two neurobiological factors and, in some cases, their interaction with a limited number of environmental factors. However, from a biopsychosocial perspective, it is critical to integrate neurobiological assessments with the primarily psychosocial assessments used in current clinical practice. Studies have shown that such an integrated approach can significantly improve the prediction of reoffending. Furthermore, it may provide a more nuanced understanding of the underlying mechanisms involved in different subtypes of antisocial behavior, such as the group exhibiting severe and persistent antisocial behavior alongside CU traits.

Secondly, most existing findings are based on group-level analyses, making it challenging to translate them into interventions tailored to individuals. By implementing structured biopsychosocial assessments in clinical settings, longitudinal data can be collected to develop open-source models and algorithms for predicting individual treatment outcomes.

Thirdly, while some evidence suggests that interventions can modify neurobiological characteristics, more knowledge is needed on the extent to which the neurodevelopmental and neurobiological features of antisocial youth can be changed through treatment. This fundamental understanding is crucial for determining whether sufficient neuroplasticity exists to redirect early antisocial development towards a more positive trajectory.

In conclusion, this review highlights the wealth of knowledge available on the genetic, neuroimaging, neuropsychological, neurophysiological, and neuroendocrinological correlates of antisocial behavior in adolescents. However, it also underscores that to advance the field and ensure direct clinical relevance, future research on the neurobiology of antisocial behavior should prioritize the integration of neurobiological findings into clinical practice. This integration will allow for the study of individual biopsychosocial profiles and their responsiveness to treatment. Achieving this goal necessitates a collaborative, translational, and iterative approach involving both researchers and clinicians. We need to move beyond mere observation and actively intervene in clinical settings to gain a deeper understanding of this complex phenomenon.

The goal is to establish a translational research cycle encompassing the consolidation of existing knowledge, translation of this knowledge into integrated assessments, interventions, and educational materials, implementation of this integrated knowledge in clinical settings, monitoring of its application, and rigorous evaluation of its validity, usability, and effectiveness. Importantly, this cycle is dynamic, acknowledging that fundamental knowledge is constantly evolving and that information flows bidirectionally between research and clinical practice. Ultimately, this collaborative effort will enable us to translate fundamental neurobiological research into personalized treatment programs tailored to the unique biopsychosocial profiles of antisocial youth.

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Introduction

Teenagers are in a state of figuring out who they are and testing boundaries, which sometimes means taking risks. Many teens engage in antisocial behavior – like aggression, breaking rules, or other actions that hurt others – at some point. Usually, it's just a one-time thing. But some teens show a consistent pattern of antisocial behavior, often starting in early adolescence or even childhood. Many of these teens who frequently violate others' rights and disregard social rules are diagnosed with conduct disorder (CD). The most serious and persistent forms of CD often involve psychopathic traits, particularly callous-unemotional (CU) traits. Teens with CU traits lack empathy and guilt, have shallow emotions, and these traits often continue into adulthood. To help these teens and prevent long-term problems, we need to understand what causes this severe form of antisocial behavior.

Antisocial behavior is considered a problem that develops over time, caused by a mix of biological differences in the brain, psychological and cognitive factors, and difficult social experiences. Studying the brain is crucial for assessing and treating antisocial behavior. It may also help us understand different types of antisocial behavior. For example, impulsive antisocial behavior might be linked to reactive aggression and poor decision-making, suggesting problems with how the front part of the brain works. In contrast, severe and persistent antisocial behavior with CU traits is linked to planned aggression, reduced responses to distress, and a lack of emotions, suggesting problems with a part of the brain called the amygdala. However, despite all the research, current assessments and treatments for young people mainly focus on psychological, social, and environmental factors.

This review aims to summarize what we currently know about the brains of adolescents with antisocial behavior and discuss how this knowledge can be used in real-life settings.

The Brain and Antisocial Behavior

Genetics

Many studies have investigated the role of genes and environment in antisocial behavior. Recent findings show that persistent delinquency is strongly influenced by genes (67% heritability), aggressive behavior has a moderate genetic influence (39–46%), and conduct disorder in adolescence is about 50% genetic.

Specific genes related to dopamine, serotonin, and oxytocin have been linked to antisocial behavior, particularly in individuals with a history of child abuse. However, large-scale genetic studies haven't found strong and consistent links between specific genes and antisocial behavior. Antisocial behavior is likely influenced by many genes, each with a small effect, and strongly influenced by environmental factors. A newer approach, polygenic risk score (PRS), looks at the combined effect of many genes. Recent studies show that PRS can differentiate between stable low and high aggressive behavior during adolescence. These studies confirm the involvement of genes related to glutamate, dopamine, and hormones in aggression and CU traits.

Neuroimaging

Brain imaging studies have taught us a lot about how the brain develops during adolescence. They show that the risky behavior typical in many teens is partly due to the slower development of the brain's control systems in the front part of the brain, compared to the faster development of emotional and social systems in deeper brain areas. For most teens, this behavior is temporary and specific to adolescence. However, studies on teens with severe and persistent antisocial behavior, including those with CD and/or CU traits, reveal specific brain differences, particularly in the prefrontal cortex, subcortical areas (like the amygdala), and the connections between them.

Firstly, brain imaging studies show that individuals with a family history of CD have smaller volumes in specific brain regions. These areas include the frontal lobe, superior temporal gyrus, (inferior) parietal lobe, and occipital lobe, as well as the cingulate cortex. There's also evidence that childhood maltreatment in those with CD is linked to specific gray matter changes in frontal and limbic regions. Although there's limited evidence for structural brain abnormalities in those with CU traits, some studies suggest specific differences in limbic and paralimbic structures. As for the connections between brain areas, aggression has been linked to reduced white matter density in pathways connecting subcortical and cortical regions. CD and CU traits are linked to changes in key connections, including the cingulum (in males with CD) and the corpus callosum, anterior thalamic radiation, and uncinate fasciculus (in those with CU traits).

Functional MRI studies show that severe antisocial behavior is also linked to unusual activity in subcortical areas related to emotions. This includes differences in how the striatum and orbitofrontal cortex (OFC) function in reward processing compared to typically developing youth. There are also differences in amygdala activity during the processing of emotional faces, empathy, and threat, particularly in youth with high CU traits. Finally, studies on resting-state brain activity suggest that CD is characterized by different connectivity patterns in the default mode network, sensorimotor networks, and the limbic system. Proactive aggression and CU traits were linked to specific connectivity patterns in areas associated with emotion, empathy, morality, and cognitive control, including the amygdala and precuneus, as well as frontal, parietal, and cingulate areas.

Neuropsychology

Generally, young offenders show some level of impairment in their cognitive functioning. Adolescents with antisocial and psychopathic traits often have lower IQs, especially lower verbal IQs.

Regarding specific neuropsychological deficits, the observed patterns in antisocial behavior align with the structural and functional brain differences discussed earlier. The most consistent finding is the presence of problems with executive functions (EF). Executive functions are mental processes that help us adapt our behavior to new situations. Deficits in EF, such as response inhibition, working memory, and mental flexibility, have been observed in both CD and young adults with psychopathic traits. EF dysfunctions might also explain the link between traumatic brain injuries and antisocial behavior. Executive functions, including social attention, cognitive flexibility, working memory, and social planning, are crucial for emotional and social skills. Regarding emotion processing, specific deficits in emotion recognition, emotional learning, and emotion regulation have been found in youth with CD, and these deficits might be linked to CU traits. However, it is important to note that not all studies show a direct link between these emotional processing difficulties and CU traits in CD.

Neurophysiology and Neuroendocrinology

The autonomic nervous system (ANS) is frequently studied in relation to antisocial behavior. The low-arousal theory suggests that antisocial behavior is linked to low ANS activity, which might lead to sensation-seeking and fearlessness. A comprehensive meta-analysis found that low resting heart rate is the most reliable indicator of antisocial behavior throughout adolescence and early adulthood, with stronger effects in groups with more serious antisocial behaviors, such as serious offenders and those with psychopathic traits. However, these findings have not been consistently replicated in all studies. This inconsistency could be due to the differences within CD itself. For instance, teens with high CU traits and proactive aggression tend to have low arousal levels, while those with more anxiety and reactive aggression display high arousal.

Heart Rate Variability (HRV) is a measure of the variation in time between each heartbeat. One type of HRV, called Respiratory Sinus Arrhythmia (RSA), is often studied as an indicator of emotion regulation. Several studies show a reduced RSA response to various emotional stimuli in individuals with antisocial behavior, although these findings are less consistent than those for resting heart rate.

Many studies have focused on stress reactivity in antisocial behavior, often measuring heart rate and cortisol (a stress hormone). These studies also found a blunted stress response in adolescents with antisocial disorders, particularly in those with CU traits. Moreover, the dorsal striatum, part of the brain's reward system and sensitive to adversity, seems to play a role in cortisol responses specifically related to externalizing behavior. However, a recent review found inconsistent results when examining the relationship between basal and reactive cortisol levels and the development of delinquent behavior.

Lastly, sex hormones, especially testosterone in males, have been linked to aggressive behavior and CD.

A recent large-scale study combining neurophysiological and neuroendocrinological assessments across several groups of antisocial and typically developing individuals confirmed the importance of these measures. Both neurophysiology and neuroendocrinology are linked to antisocial behavior, including psychopathic traits, aggression, and impulsivity. These relationships remain consistent throughout adolescence and early adulthood.

Using Brain Science in Real-World Settings with Young Offenders

Diagnostics and Risk Assessment

Based on current knowledge, using brain science to distinguish between antisocial behavior with or without psychopathic traits, particularly CU traits, can be incredibly valuable in real-world settings. Neurobiological assessments might provide objective measures of CU traits, going beyond self-report alone. Based on current research, the most promising assessments for differentiating between antisocial youth with or without CU traits are:

• Neurophysiological measures: Heart rate, heart rate variability/RSA.

• Neuroendocrinological measures: Cortisol, testosterone.

• Neuropsychological assessments: Emotion recognition, emotional learning, and emotion regulation.

These measures are linked to stress and emotional processing, as well as to brain differences in areas like the amygdala in antisocial youth with CU traits. Assessing executive function, crucial for emotional and social skills, is also important.

However, it's crucial to remember that neurobiological assessments should be combined with psychosocial assessments, as many studies have found a link between parental antisocial behavior, harsh parenting, maltreatment, and altered heart rate and RSA levels in antisocial youth, with or without CU traits. This might indicate potential pathways through which genes and early adversity impact the development of antisocial behavior and CU traits, as proposed by Blair's neurobiological model of psychopathy development.

Regarding risk assessment, recent studies have shown that incorporating neurophysiological and neuroendocrinological measures into standard assessments significantly improves the prediction of re-offending (including violent re-offending) in severely antisocial and delinquent youth.

Treatment and Treatment Evaluation

The biggest challenge is translating our understanding of the brain into effective interventions for young people with antisocial behavior.

First, brain science is valuable for educating both youth and their parents. Understanding the biological processes underlying their behavior can help young people make sense of their actions. However, it is crucial to emphasize that despite the significant role of genetics in antisocial behavior and brain development, this doesn't mean that individuals are predestined to commit crimes. While heritability might be high, environmental factors still play a significant role. Moreover, the adolescent brain is still developing and adaptable, providing a window of opportunity for interventions to redirect antisocial trajectories.

Second, neurobiological findings can guide the development of interventions to change the developmental trajectory of antisocial behaviors. For severely delinquent youth, understanding the brain can help develop effective interventions within the juvenile justice system.

Examples of neurobiologically informed interventions include:

• Pharmacological interventions: Medications targeting dopamine, norepinephrine, and serotonin, such as psychostimulants, alpha-2 agonists, atomoxetine, and risperidone, have shown some benefits. Specifically, methylphenidate might normalize amygdala function and resting-state functional connectivity in adolescents with conduct disorder, areas linked to antisocial behavior and CU traits.

• Cognitive training: Interventions aimed at improving executive functioning, such as cognitive training and enhancing cognitive control, are promising. Specifically, training executive functions combined with parental training in perseverance may reduce proactive aggression. Recently, a program tailoring interventions to individual neuropsychological profiles effectively reduced antisocial behavior in high-risk children.

• Aggression management: Programs like Triple P and Aggression Replacement Therapy (ART) have been shown to reduce aggression by improving self-control. ART has even been shown to normalize neuroendocrine functioning in antisocial youth, including those with CU traits.

• Biofeedback: Using wearable technology to increase awareness of physiological signals preceding aggressive outbursts and promoting emotion and aggression regulation is a promising approach.

Translational Research Agenda

While we've gained considerable knowledge about the brain and antisocial behavior, some knowledge gaps hinder its full application in real-world settings.

First, we need to understand how biological, psychological, and social factors interact. Current research mainly focuses on one or two neurobiological factors, sometimes in combination with a few environmental factors. However, a comprehensive understanding requires integrating neurobiological assessments with the psychosocial assessments used in clinical practice. This integrated approach has shown great promise in improving re-offending predictions and might provide a deeper understanding of the mechanisms underlying different antisocial behavior subtypes.

Second, most research findings are based on group averages, making it difficult to apply them to individual cases. By collecting longitudinal data on individuals through integrated biopsychosocial assessments in clinical settings, we can develop models and algorithms to predict individual treatment outcomes.

Third, while some evidence suggests that interventions can change brain characteristics, we need more research on how adaptable these characteristics are in response to treatment. This is crucial for understanding whether enough neuroplasticity exists to alter the course of antisocial development.

To conclude, we have a wealth of knowledge about the brain and antisocial behavior. However, to maximize clinical relevance, future research must focus on integrating neurobiological research into clinical practice. This will allow us to study individual biopsychosocial profiles and how adaptable they are to treatment. To achieve this, we need a collaborative, translational approach involving researchers and clinicians. This involves a continuous cycle of:

• Consolidating knowledge: Combining and strengthening existing research findings.

• Translating knowledge: Applying this knowledge to develop integrated assessments, interventions, and educational materials.

• Implementing knowledge: Putting these tools into practice in real-world settings.

• Monitoring use: Tracking how these tools are used in clinical practice.

• Evaluating effectiveness: Assessing the validity, usability, and impact of these tools.

This cycle is dynamic, meaning that new research continually updates our understanding, and information flows both ways between research and clinical practice. This collaborative approach will ultimately help us translate our understanding of the brain into personalized treatment programs tailored to the unique profiles of young people with antisocial behavior.

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Introduction

Trying new things and sometimes taking risks is a normal part of growing up. Many teens and kids might show some not-so-good behaviors (like being aggressive, breaking rules, or doing things that are wrong) at some point. Usually, this only happens once or twice. But some kids keep showing these behaviors, and they might even start doing them at a young age.

When teens constantly break rules, hurt others, and don't follow the rules of society, they might have a "conduct disorder." Some of these teens also have something called "callous-unemotional" traits, or "CU traits." These kids don't feel bad when they do something wrong, and they don't care about other people's feelings. This can make their behavior even more worrisome.

To help these teens make better choices, we need to understand what's happening in their brains and why they act this way.

What Makes Some Teens Behave Badly?

Scientists believe that bad behavior in teens is a problem that starts developing early on. It's caused by a mix of things happening in their brains, their thoughts and feelings, and their experiences in life.

It's in the genes: Just like we inherit our parents' hair color, we might also inherit certain ways our brains are wired. These can make us more likely to behave in certain ways. Studies show that genes play a big part in why some kids struggle with following rules.

Looking inside the brain: Scientists use special tools to take pictures of the brain and see how it's working. They've discovered that kids who break rules a lot often have some differences in certain parts of their brains. These differences can affect how they control their impulses, understand emotions, and make decisions.

Thinking and feeling differently: Kids who break rules often have trouble with things like paying attention, controlling their impulses, and understanding other people's feelings. This makes it hard for them to make good choices and learn from their mistakes.

Tough times in life: Sometimes, bad things happen to kids, like abuse or neglect. These experiences can make it even harder for them to cope with their emotions and behave in positive ways.

How Can We Use This Knowledge to Help?

Figuring out the problem: Doctors and other professionals can use this information about the brain and behavior to better understand why a child is acting out. This can help them figure out the best way to help.

Teaching kids about their brains: Explaining to teens how their brains work can help them understand why they might be struggling with certain behaviors. It's important to remember that even though our brains play a big role in how we act, we can still learn to make better choices!

Finding the right help: Knowing more about a the brain and behavior can help professionals develop specific treatments and therapies that address their individual needs. This might include things like therapy to help them manage their emotions, medication to help with attention or impulsivity, or programs to teach them new skills.

Helping families: It's important for families to understand that bad behavior is often a sign that a child is struggling. Professionals can work with families to teach them how to support their child and create a positive home environment.

Scientists are still learning a lot about the brain and behavior, but what they're finding out is already making a difference in the lives of teens who struggle with antisocial behavior.

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