Considerable effort has been devoted to understanding how parents influence child development. Less attention has been given to the effects that children exert on their parents. This review aims to systematically survey the links between scientific articles exploring this question. Results of a document co-citation analysis reveal that research on this topic has been scarce and primarily concerned by how child and adolescent disruptive behaviour negatively impacts parents. Academic attention is directed to research that conceptualizes child effects as the outcome of genetic or temperamental predispositions. The implications of such a constrained view of child influence are discussed, highlighting the need for applied research on how children can actively contribute to positive behavioural change in parents and other adults.

The first signs of mental health issues in dentistry manifest as early as undergraduate training, thus it is essential to delve into the concept of resilience to equip those studying and working in dentistry with the resources to cultivate a positive mindset.

A focus group was conducted with a homogenous purposive sample of eight undergraduate dental profession students from all 3 years of study at the University of Portsmouth Dental Academy (UPDA). The six-phase Braun and Clarke's thematic analysis was adopted to interpret patterns in data.

Four themes of: 'definition of resilience'; 'factors enhancing resilience'; 'factors challenging resilience' and 'developing resilience in dentistry'; and 23 subthemes were identified. Students defined resilience as an ability to bounce back from adversity and perceived it as a dynamic and contextual phenomenon that fluctuated due to an interplay of personal, social and environmental factors.

The findings of this study showed undergraduate dental profession students' perceptions of resilience, factors influencing it and strategies to develop it. These findings may inform the curriculum of resilience training programmes targeted towards this population.

The analysis of citation flow from a collection of scholarly articles might provide valuable insights into their thematic focus and the genealogy of their main concepts. In this study, we employ a topic model to delineate a subcorpus of 1,360 papers representative of bioethical discussions on enhancing human life. We subsequently conduct an analysis of almost 11,000 references cited in that subcorpus to examine quantitatively, from a bird's-eye view, the degree of openness of this part of scholarship to the specialized knowledge produced in biosciences. Although almost half of the analyzed references point to journals classified as Natural Science and Engineering (NSE), we do not find strong evidence of the intellectual influence of recent discoveries in biosciences on discussions on human enhancement. We conclude that a large part of the discourse surrounding human enhancement is inflected with "science-fictional habits of mind." Our findings point to the need for a more science-informed approach in discussions on enhancing human life.

Anti-social behavior and violence are major public health concerns. Globally, violence contributes to more than 1.6 million deaths each year. Previous studies have reported that social rejection or neglect exacerbates aggression. In rodent models, social isolation stress is used to demonstrate the adverse effects of social deprivation on physiological, endocrinological, immunological, and behavioral parameters, including aggressive behavior. This review summarizes recent rodent studies on the effect of social isolation stress during different developmental periods on aggressive behavior and the underlying neural mechanisms. Social isolation during adulthood affects the levels of neurosteroids and neuropeptides and increases aggressive behavior. These changes are ethologically relevant for the adaptation to changes in local environmental conditions in the natural habitats. Chronic deprivation of social interaction after weaning, especially during the juvenile to adolescent periods, leads to the disruption of the development of appropriate social behavior and the maladaptive escalation of aggressive behavior. The understanding of neurobiological mechanisms underlying social isolation-induced escalated aggression will aid in the development of therapeutic interventions for escalated aggression.

Reducing the risk of aggressive behaviour requires preventive measures that depend on our knowledge of predisposing factors. The study's aim was to compare sociodemographic variables, clinical variables and the frequency of gene polymorphisms predisposing to destructive behaviour between subpopulations of individuals with a history of suicidality and/or of aggression, both being treated for alcohol dependence.

Sixty-nine patients hospitalised for alcohol dependence participated in the study. The sociodemographic, clinical (SADD, BPAQ) and genetic variables were compared between subpopulations of alcohol-dependent patients selected according to type of aggressive behaviour, including a history of suicidal behaviour and control nonalcohol-dependent group. Polymorphisms of MAOA, COMT, DRD2 and DAT1 loci that are known as risk factors of mental dysfunctions were investigated.

The subpopulation of patients with suicide attempts had a longer time in education than patients with aggressive and suicidal behaviour (11.9 vs 9.7 years). Patients with suicide attempts and patients with aggression had lower levels of alcohol dependence than patients with comorbid suicide attempts and concomitant aggression. For the MAOA gene lower frequency of the G/G genotype with tendency to statistical significance was observed among patients burdened by suicidal behaviour in comparison to patients with aggression and a significantly higher A/G genotype compared to cases with aggression and controls. In the case of COMT polymorphism, the G/G genotype was reported significantly less often among patients with suicide attempts and comorbid aggression than among patients with control group).

Compared to patients with either only suicidal tendencies or aggression, those with comorbid aggression and suicide attempts are characterised by poorer social performance. Genetic variation in MAOA loci may be a risk factor for impulsive behaviour like suicidal behaviour, and especially aggression.

Leveraging real-world clinical biobanks to investigate the associations between genetic and environmental risk factors for mental illness may help direct clinical screening efforts and evaluate the portability of polygenic scores across environmental contexts.

To examine the associations between sexual trauma, polygenic liability to mental health outcomes, and clinical diagnoses of schizophrenia, bipolar disorder, and major depressive disorder in a clinical biobank setting.

This genetic association study was conducted using clinical and genotyping data from 96 002 participants across hospital-linked biobanks located at Vanderbilt University Medical Center (VUMC), Nashville, Tennessee (including 58 262 individuals with high genetic similarity to the 1000 Genomes Project [1KG] Northern European from Utah reference population [1KG-EU-clustered] and 11 047 with high genetic similarity to the 1KG African-ancestry reference population of Yoruba in Ibadan, Nigeria [1KG-YRI-clustered]), and Mass General Brigham (MGB), Boston, Massachusetts (26 693 individuals with high genetic similarity to the combined European-ancestry superpopulation [1KG-EU-clustered]). Clinical data analyzed included diagnostic billing codes and clinical notes spanning from 1976 to 2023. Data analysis was performed from 2022 to 2024.

Clinically documented sexual trauma disclosures and polygenic scores for schizophrenia, bipolar disorder, and major depressive disorder.

Diagnoses of schizophrenia, bipolar disorder, and major depressive disorder, determined by aggregating related diagnostic billing codes, were the dependent variables in logistic regression models including sexual trauma disclosure status, polygenic scores, and their interactions as the independent variables.

Across the VUMC and MGB biobanks, 96 002 individuals were included in analyses (VUMC 1KG-EU-clustered: 33 011 [56.7%] female; median [range] age, 56.8 [10.0 to >89] years; MGB 1KG-EU-clustered: 14 647 [54.9%] female; median [range] age, 58.0 [10.0 to >89] years; VUMC 1KG-YRI-clustered: 6961 [63.0%] female; median [range] age, 44.6 [10.1 to >89] years). Sexual trauma history was associated with all mental health conditions across institutions (ORs ranged from 8.83 [95% CI, 5.50-14.18] for schizophrenia in the VUMC 1KG-YRI-clustered cohort to 17.65 [95% CI, 12.77-24.40] for schizophrenia in the VUMC 1KG-EU-clustered cohort). Sexual trauma history and polygenic scores jointly explained 3.8% to 8.8% of mental health phenotypic variance. Schizophrenia and bipolar disorder polygenic scores had greater associations with mental health outcomes in individuals with no documented disclosures of sexual trauma (schizophrenia interaction: OR, 0.70 [95% CI, 0.56-0.88]; bipolar disorder interaction: OR, 0.83 [95% CI, 0.74-0.94]).

Sexual trauma and mental health polygenic scores, while correlated with one another, were independent and joint risk factors for severe mental illness in a large, diverse hospital biobank population. Furthermore, associations of schizophrenia and bipolar disorder polygenic scores with respective diagnoses were greater in those without disclosures, suggesting that genetic predisposition to mental illness as measured by polygenic scores may be less impactful in the presence of this severe environmental risk factor.

Antisocial behavior (ASB) refers to a set of behaviors that violate social norms and disregard the well-being and rights of others. In this review, we synthesize evidence from studies using genetically informed designs to investigate the genetic and environmental contributions to individual differences in ASB. We review evidence from studies using family data (twin and adoption studies) and measured DNA (candidate gene and genome-wide association studies) that have informed our understanding of ASB. We describe how genetically informative designs are especially suited to investigate the nature of environmental risk and the forms of gene-environment interplay. We also highlight clinical and legal implications, including how insights from genetically informed research can help inform prevention and intervention, and we discuss some challenges and opportunities within this field of research.

To produce a theoretical approach about the relations between neuroscience and psychopathology that expands beyond the biomedical model to include a non-reductionist, enactive, and biocultural perspective. An integrative review, drawing from the biocultural approach from Anthropology, is used to produce examples from epigenetics, neuroplasticity, and functional neuroanatomy. A biocultural approach points to a brain that is highly plastic, reinforcing a much more complex model in which biological vulnerabilities and the historical-cultural environment co-construct each other. The examples given seem to point to the pressing need for a critical expansion of reductionist models of psychopathology. Importantly, the cultural-historical environment to which we refer is not a set of neutral social relations to which individuals are homogeneously exposed, such that aspects that are usually studied under the social determinants of health and disease (poverty, discrimination, violence, and other factors that represent sources of control, production, and distribution of material resources, ideology, and power) need to be incorporated in adequate biopsychosocial models of mental distress.

Individuals with autism spectrum disorder (ASD) are more likely to experience adverse childhood experiences (ACEs) compared with typically developing (TD) individuals, which predisposes them to an elevated risk of mental health issues. This review elucidates the profound impact of ACEs on individuals with ASD by synthesizing findings from a plethora of epidemiologic and biological studies, encompassing genetics, epigenetics, and neuroimaging. Despite the limited number of studies explicitly focusing on this intersection, the extant literature consistently demonstrates that ASD individuals are disproportionately affected by ACEs, leading to significant deterioration in mental health and brain function. Furthermore, the nature and extent of the effects of ACEs appear to diverge between ASD and TD populations, underscoring the necessity for tailored clinical and research approaches. Understanding these complex and intertwined interactions is imperative for advancing both clinical practice and research, with the goal of mitigating the adverse outcomes associated with ACEs in ASD individuals.

Brunner syndrome is a rare genetic disorder that associated with mutations in the MAOA gene. It has been linked to a number of psychiatric disorders. We present detailed information on psychiatric evaluation of a case carrying a novel MAOA gene variant of p.(Thr408Met). The patient was referred to our clinic with a history of attention problems, motor coordination difficulties and a tendency to bite objects. Following a comprehensive psychiatric evaluation, the patient was diagnosed with developmental coordination disorder, articulation disorder and attention deficit hyperactivity disorder (ADHD). MAOA mutations are rarely reported in the literature. To date, a total of 23 MAOA gene variants, mostly missense variants, have been reported through the HGMD database (Professional 2023.4). Neurodevelopmental symptoms may vary in severity and diversity among patients with Brunner syndrome. Different degrees of intellectual disability have been found in previously reviewed cohorts of Brunner syndrome. In our affected patient, cognitive development and academic achievement were at a similar level to his peers. Additionally, our patient exhibited symptoms suggestive of developmental coordination disorder. Our findings show that genetic mutations in MAOA can lead to a wide range of clinical symptoms and underline the need for comprehensive genetic and clinical evaluations.

In this essay, I will briefly sample different instances of the utilization of the concept of resilience, attempting to complement a comprehensive representation of the field in the special issue of Development and Psychopathology inspired by the 42nd Minnesota Symposium on Child Psychology, hosted by the Institute of Child Development at the University of Minnesota and held in October of 2022. Having established the general context of the field, I will zoom in on some of its features, which I consider "low-hanging fruit" and which can be harvested in a systematic way to advance the study of resilience in the context of the future of developmental psychopathology.

This is the first episode of a series of four discussions on the differences between males and females, in apparently non-andrological fields. You will read the transcript of discussions that actually took place at the Endocrinology Unit in Modena, Italy, in the form of the aporetic dialogues of ancient Greece. In this episode, the role of testosterone in gender differences in criminal behavior will be explored. The discussants were divided into two groups: group 1, which supports the thesis of a predominant role of testosterone, and group 2, which opposes it. The first group affirmed that both endogenous testosterone and anabolic-androgenic steroids could trigger aggressive and criminal behavior, regardless of predisposition to psychiatric disease or sociocultural background. The second group asserted the multifactorial genesis of aggressive and criminal behavior, citing other hormonal and non-hormonal factors, such as neurotransmitters, cortisol, and sociological and psychological aspects. In the end, a forensic physician, acting as a referee, tried to resolve the aporia: are the two theories equivalent or one is superior?

This study aims to explore the concept of future orientation, which encompasses individuals' thoughts about the future, goal-setting, planning, response to challenges and behavioural adjustments in evolving situations. Often viewed as a psychological resource, future orientation is believed to be developed from psychological resilience. The study investigates the curvilinear relationship between childhood maltreatment and future orientation while examining the moderating effects of genotype.

A total of 14,675 Chinese adults self-reported their experiences of childhood maltreatment and their future orientation. The influence of genetic polymorphism was evaluated through genome-wide interaction studies (GWIS; genome-wide association study [GWAS] using gene × environment interaction) and a candidate genes approach.

Both GWAS and candidate genes analyses consistently indicated that rs4498771 and its linked single-nucleotide polymorphisms, located in the intergenic area surrounding CSF3R, significantly interacted with early trauma to influence future orientation. Nonlinear regression analyses identified a quadratic or cubic association between future orientation and childhood maltreatment across some genotypes. Specifically, as levels of childhood maltreatment increased, future orientation declined for all genotypes. However, upon reaching a certain threshold, future orientation exhibited a rebound in individuals with specific genotypes.

The findings suggest that individuals with certain genotypes exhibit greater resilience to childhood maltreatment. Based on these results, we propose a new threshold model of stress-related growth.

Major depressive disorder (MDD) is a debilitating mental illness, and it is considered to be one of the leading causes of disability globally. The etiology of MDD is multifactorial, involving an interplay between biological, psychological, and social factors. Early life represents a critical period for development. Exposure to adverse childhood experiences is a major contributor to the global burden of disease and disability, doubling the risk of developing MDD later in life. Evidence suggests that stressful events experienced during that timeframe play a major role in the emergence of MDD, leading to epigenetic modifications, which might, in turn, influence brain structure, function, and behavior. Neuroplasticity seems to be a primary pathogenetic mechanism of MDD, and, similarly to epigenetic mechanisms, it is particularly sensitive to stress in the early postnatal period. In this review, we will collect and discuss recent studies supporting the role of epigenetics and neuroplasticity in the pathogenesis of MDD, with a focus on early life stress (ELS). We believe that understanding the epigenetic mechanisms by which ELS affects neuroplasticity offers potential pathways for identifying novel therapeutic targets for MDD, ultimately aiming to improve treatment outcomes for this debilitating disorder.

Antisocial personality disorder (ASPD) is a characterized by lifelong or recurrent behavioral problems that begin in childhood or early adolescence. This communication provides an overview on ASPD including findings from recent reviews and new research.

With regard to DSM-5's Section III Alternative Model of Personality Disorder criteria for ASPD, advocates point to the broader symptom coverage and harmonization with ICD-11; yet critics point to the lack of evidence for improved outcomes. A new report shows that antisocial individuals age faster than non-antisocial peers. ASPD has high heritability and newer molecular studies have found intriguing linkages to genes associated with crucial brain regions. A mentalization-based therapy model has been developed and early work shows promise. ASPD is common, widespread, and disruptive to individuals, families, and society. Chronic and lifelong, ASPD typically lessens in severity with advancing age. Assessment rests on the individual's history because there are no diagnostic tests. ASPD likely results from an interplay of genetic and environmental factors. Brain imaging studies have linked cortical dysfunction to antisocial behavior in crucial brain regions. Medication is sometimes targeted at the individual's aggression and irritability, but a more rational approach is to target co-occurring disorders. Cognitive-behavioral therapy and mentalization-based therapy models have been developed and are being studied.

Reinforcement sensitivity is a hypothesized attention-deficit/hyperactivity disorder (ADHD) intermediate phenotype but its role in transgenerational transmission of ADHD-linked psychopathology risk is largely unknown. We examined, in a carefully phenotyped, N = 123 sample of adolescents (Mage = 15.27 years, SD = 0.984; 61.78% boys), whether (1) parental psychopathology is differentially associated with fMRI-indexed neural response to reward receipt and (2) both maternal and paternal psychopathology are associated with neural response to reward; across adolescents at-risk for and not at-risk for ADHD. Indices of parental psychopathology were differentially associated with adolescent offspring neural response to reward such that across measures, parental psychopathology was negatively or not associated with offspring superior frontal gyrus (SFG) response to reward receipt in adolescents at-risk for ADHD, but parental psychopathology was positively associated with offspring SFG response in adolescents not at-risk. Further, across measures, greater maternal psychopathology was associated with blunted adolescent SFG response to reward in adolescents at-risk for ADHD whereas greater maternal externalizing problems were linked to enhanced adolescent SFG response in adolescents not at-risk. Across measures, paternal psychopathology was not associated with adolescent response to reward, in either group. ADHD risk confers differential reward-related susceptibility to the effects of parental psychopathology. Results also show this association is nonspecific in terms of parental psychopathology type but is specific to maternal psychopathology.

Background: Coping with stress is essential for mental well-being and can be critical for highly sensitive individuals, characterized by a deeper perception and processing of stimuli. So far, the molecular bases characterizing high-sensitivity traits have not been completely investigated and gene × environment interactions might play a key role in making some people more susceptible than others. Methods: In this study, 104 young adult university students, subjects that might face overwhelming experiences more than others, were evaluated for the genetics and epigenetics of dopamine (DAT1) and serotonin (SERT) transporter genes, in addition to the expression of miR-132, miR-491, miR-16, and miR-135. Results: We found an increase in DNA methylation at one specific CpG site at DAT1 5'UTR in highly sensitive students reporting high levels of perceived stress when compared to those less sensitive and/or less stressed. Moreover, considering DAT1 VNTR at 3'UTR, we observed that this effect was even more pronounced in university students having the 9/9 genotype when compared to those with the 9/10 genotype. These data are corroborated by the higher levels of miR-491, targeting DAT1, in highly sensitive subjects with high levels of perceived stress. SERT gene DNA methylation at one specific CpG site was reported to instead be higher in subjects reporting lower perceived stress when compared to more stressed subjects. Consistently, miR-135 expression, regulating SERT, was lower in subjects with higher perceived stress. Conclusions: We here suggest that the correlation of DAT1 and SERT genetic and epigenetic data with the analysis of stress and sensitivity might be useful to suggest possible biomarkers to monitor mental health wellness in vulnerable subjects.

Stress profoundly affects physical and mental health, particularly when experienced early in life. Early-life stress (ELS) encompasses adverse childhood experiences such as abuse, neglect, violence, or chronic poverty. These stressors can induce long-lasting changes in brain structure and function, impacting areas involved in emotion regulation, cognition, and stress response. Consequently, individuals exposed to high levels of ELS are at an increased risk for mental health disorders like depression, anxiety, and post-traumatic stress disorders, as well as physical health issues, including metabolic disorders, cardiovascular disease, and cancer. This review explores the biological and psychological consequences of early-life adversity paradigms in rodents, such as maternal separation or deprivation and limited bedding or nesting. The study of these experimental models have revealed that the organism's response to ELS is complex, involving genetic and epigenetic mechanisms, and is associated with the dysregulation of physiological systems like the nervous, neuroendocrine, and immune systems, in a sex-dependent fashion. Understanding the impact of ELS is crucial for developing effective interventions and preventive strategies in humans exposed to stressful or traumatic experiences in childhood.

With high rates of violence exposure among justice-involved youth, it is critical to identify factors that might impact the likelihood of youth engaging in violence themselves. One such factor is sensitivity to context, which describes how sensitive youth are to experiences in their environment. Using an ethnically diverse sample of justice-involved male adolescents (47% Latino, 38% Black/African American, 15% White) aged 13-17 at the time of their first arrest, the results of this study indicate that exposure to violence was related to increased violent behavior six months later, and this effect was strongest among youth who were low in sensitivity to context. These findings may help practitioners identify which youth are at greatest risk for violence in a policy-relevant population.

Recent shifts in societal attitudes towards cannabis have led to a dramatic increase in consumption rates in many Western countries, particularly among young people. This trend has shed light on a significant link between cannabis use disorder (CUD) and pathological reactive aggression, a condition involving disproportionate aggressive and violent reactions to minor provocations. The discourse on the connection between cannabis use and aggression is frequently enmeshed in political and legal discussions, leading to a polarized understanding of the causative relationship between cannabis use and aggression. However, integrative analyses from both human and animal research indicate a complex, bidirectional interplay between cannabis misuse and pathological aggression. On the one hand, emerging research reveals a shared genetic and environmental predisposition for both cannabis use and aggression, suggesting a common underlying biological mechanism. On the other hand, there is evidence that cannabis consumption can lead to violent behaviors while also being used as a self-medication strategy to mitigate the negative emotions associated with pathological reactive aggression. This suggests that the coexistence of pathological aggression and CUD may result from overlapping vulnerabilities, potentially creating a self-perpetuating cycle where each condition exacerbates the other, escalating into externalizing and violent behaviors. This article aims to synthesize existing research on the intricate connections between these issues and propose a theoretical model to explain the neurobiological mechanisms underpinning this complex relationship.

Risk-allele carriers of a Monoamine oxidase A (MAOA) gene, short-allele (MAOA-S) in males and long-allele (MAOA-L) in females, in the presence of a negative environment, are associated with alcohol misuse. Whether MAOA-S/L alleles also present susceptibility to a positive environment to mitigate the risk of alcohol misuse is unknown. Thus, we assessed the association of the three-way interaction of MAOA, maltreatment, and positive parent-child relationship with alcohol consumption among adolescents.

This prospective study included 1416 adolescents (females: 59.88%) aged 16 - 19 years from Sweden, enrolled in the "Survey of Adolescent Life in Västmanland" in 2012. Adolescents self-reported alcohol consumption, maltreatment by a family (FM) or non-family member (NFM), parent-child relationship, and left saliva for MAOA genotyping.

We observed sex-dependent results. Females carrying MAOA-L with FM or NFM and a good parent-child relationship reported lower alcohol consumption than those with an average or poor parent-child relationship. In males, the interactions were not significant. Results suggest MAOA-L in females, conventionally regarded as a "risk", is a "plasticity" allele as it is differentially susceptible to negative and positive environments. Results highlight the importance of a good parent-child relationship in mitigating the risk of alcohol misuse in maltreated individuals carrying genetic risk. However, the interactions were not significant after adjusting to several environmental and behavioural covariates, especially parent's alcohol use, negative parent-child relationship, and nicotine use (smoking and/or snus), suggesting predictor and outcome intersection. Future studies and frameworks for preventive strategies should consider these covariates together with alcohol consumption. More studies with larger sample sizes are needed to replicate the findings.

Traumatic stress, particularly during critical developmental periods such as adolescence, has been strongly linked to an increased propensity and severity of aggression. Existing literature underscores that being a victim of abuse can exacerbate aggressive behaviors, with the amygdala playing a pivotal role in mediating these effects. Historically, animal models have demonstrated that traumatic stressors can increase attack behavior, implicating various amygdala nuclei. Building on this foundation, our previous work has highlighted how traumatic stress invokes long-lasting aggression via an excitatory pathway within the posterior ventral medial amygdala (MeApv). In the current study, we sought to further delineate this mechanism by examining the effects of acute social defeat during adolescence on aggressive behaviors and neural activation in mice. Using a common social defeat paradigm, we first established that acute social defeat during late adolescence indeed promotes long-lasting aggression, measured as attack behavior 7 days after the defeat session. Immunolabeling with c-Fos demonstrated that acute social defeat activates the MeApv and ventrolateral aspect of the ventromedial hypothalamus (VmHvl), consistent with our previous studies that used foot shock as an acute stressor. Finally, chemogenetically inhibiting excitatory MeApv neurons during social defeat significantly mitigated the aggression increase without affecting non-aggressive social behavior. These results strongly suggest that the MeApv plays a critical role in the onset of aggression following traumatic social experience, and offer the MeA as a potential target for therapeutic interventions.

The current study explored longitudinally whether oxytocin receptor gene methylation (OXTRm) changes moderated the association between parental sensitivity changes and children's attachment changes over three waves. Six hundred six Flemish children (10-12 years, 42.8%-44.8% boys) completed attachment measures and provided salivary OXTRm data on seven CpG sites. Their parents reported their sensitive parenting. Results suggest that OXTRm changes hardly link to attachment (in)security changes after the age of 10. Some support was found for interaction effects between parental sensitivity changes and OXTRm changes on attachment changes over time. Effects suggest that for children with increased OXTRm in the promotor region and decreased methylation in the inhibitor region over time, increased parental sensitivity was associated with increased secure attachment and decreased insecure attachment over time.

Post-traumatic stress symptoms (PTSS) were the most frequently reported mental health concern for youth during COVID-19, yet variations in youth's PTSS responses warrant empirical consideration. Features of the caregiving environment influence youth's responses to environmental stressors, and youth's parasympathetic nervous system regulation may qualify the magnitude and/or direction of these effects. This prospective investigation evaluated diathesis stress and differential susceptibility models of caregiving and parasympathetic influences on youth's PTSS responses to COVID-19.

Participants were 225 caregiver-youth dyads (youth 49.8% female at birth; 88.4% non-white) followed from childhood through adolescence and COVID-19. Youth's resting respiratory sinus arrhythmia (RSA; Mage = 6.11, s.d. = 0.21), caregiving features (i.e. attachment security [youth Mage = 12.24, s.d. = 0.35] and caregiver internalizing psychopathology [caregiver Mage = 39.29, s.d. = 6.78]) were assessed pre-pandemic. Youth's PTSS was assessed one year prior to the US COVID-19 pandemic (Mage = 14.24, s.d. = 0.50) and during the spring of 2020 at the height of the pandemic (Mage = 15.23, s.d. = 0.57).

Youth's PTSS increased during COVID-19. Youth with relatively high resting RSA evidenced the lowest PTSS when their caregiving environment featured high attachment security or low caregiver internalizing problems, but the highest PTSS when their caregiving environment featured low attachment security or high caregiver internalizing problems. In contrast, PTSS levels of youth with relatively low or average resting RSA did not differ significantly depending on attachment security or caregiver internalizing.

Results are consistent with a differential susceptibility hypothesis, wherein relatively high resting RSA conferred heightened sensitivity to caregiving environments in a for-better-and-for-worse manner during COVID-19.

While genetic and environmental factors have been shown as predictors of children's reading ability, the interaction effects of identified genetic risk susceptibility and the specified environment for reading ability have rarely been investigated. The current study assessed potential gene-environment (G×E) interactions on reading ability in 1477 school-aged children. The gene-environment interactions on character recognition were investigated by an exploratory analysis between the risk single-nucleotide polymorphisms (SNPs), which were discovered by previous genome-wide association studies of developmental dyslexia (DD), and parental education (PE). The re-parameterized regression analysis suggested that this G×E interaction conformed to the strong differential susceptibility model. The results showed that rs281238 exhibits a significant interaction with PE on character recognition. Children with the "T" genotype profited from high PE, whereas they performed worse in low PE environments, but "CC" genotype children were not malleable in different PE environments. This study provided initial evidence for how the significant SNPs in developmental dyslexia GWA studies affect children's reading performance by interacting with the environmental factor of parental education.

Excessive and persistent aggressiveness is the most common behavioral problem that leads to psychiatric referrals among children. While half of the variance in childhood aggression is attributed to genetic factors, the biological mechanism and the interplay between genes and environment that results in aggression remains elusive. The purpose of this systematic review is to provide an overview of studies examining the genetics of childhood aggression irrespective of psychiatric diagnosis. PubMed, PsycINFO, and MEDLINE databases were searched using predefined search terms for aggression, genes and the specific age group. From the 652 initially yielded studies, eighty-seven studies were systematically extracted for full-text review and for further quality assessment analyses. Findings show that (i) investigation of candidate genes, especially of MAOA (17 studies), DRD4 (13 studies), and COMT (12 studies) continue to dominate the field, although studies using other research designs and methods including genome-wide association and epigenetic studies are increasing, (ii) the published articles tend to be moderate in sizes, with variable methods of assessing aggressive behavior and inconsistent categorizations of tandem repeat variants, resulting in inconclusive findings of genetic main effects, gene-gene, and gene-environment interactions, (iii) the majority of studies are conducted on European, male-only or male-female mixed, participants. To our knowledge, this is the first study to systematically review the effects of genes on youth aggression. To understand the genetic underpinnings of childhood aggression, more research is required with larger, more diverse sample sets, consistent and reliable assessments and standardized definition of the aggression phenotypes. The search for the biological mechanisms underlying child aggression will also benefit from more varied research methods, including epigenetic studies, transcriptomic studies, gene system and genome-wide studies, longitudinal studies that track changes in risk/ameliorating factors and aggression-related outcomes, and studies examining causal mechanisms.

Complex traits are widely considered to be the result of a compound regulation of genes, environmental factors, and genotype-by-environment interaction (G × E). The inclusion of G × E in genome-wide association analyses is essential to understand animal environmental adaptations and improve the efficiency of breeding decisions. Here, we systematically investigated the G × E of growth traits (including weaning weight, yearling weight, 18-month body weight, and 24-month body weight) with environmental factors (farm and temperature) using genome-wide genotype-by-environment interaction association studies (GWEIS) with a dataset of 1350 cattle. We validated the robust estimator's effectiveness in GWEIS and detected 29 independent interacting SNPs with a significance threshold of 1.67 × 10-6, indicating that these SNPs, which do not show main effects in traditional genome-wide association studies (GWAS), may have non-additive effects across genotypes but are obliterated by environmental means. The gene-based analysis using MAGMA identified three genes that overlapped with the GEWIS results exhibiting G × E, namely SMAD2, PALMD, and MECOM. Further, the results of functional exploration in gene-set analysis revealed the bio-mechanisms of how cattle growth responds to environmental changes, such as mitotic or cytokinesis, fatty acid β-oxidation, neurotransmitter activity, gap junction, and keratan sulfate degradation. This study not only reveals novel genetic loci and underlying mechanisms influencing growth traits but also transforms our understanding of environmental adaptation in beef cattle, thereby paving the way for more targeted and efficient breeding strategies.

Genotype × environment interactions (GxE) have long been recognized as a key mechanism underlying human phenotypic variation. Technological developments over the past 15 years have dramatically expanded our appreciation of the role of GxE in both gene regulation and complex traits. The richness and complexity of these datasets also required parallel efforts to develop robust and sensitive statistical and computational approaches. Although our understanding of the genetic architecture of molecular and complex traits has been maturing, a large proportion of complex trait heritability remains unexplained. Furthermore, there are increasing efforts to characterize the effect of environmental exposure on human health. We therefore review GxE in human gene regulation and complex traits, advocating for a comprehensive approach that jointly considers genetic and environmental factors in human health and disease.

Cognitive behavioral therapy is based on the view that maladaptive thinking is the causal mechanism of mental disorders. While this view is supported by extensive evidence, very limited work has addressed the factors that contribute to the development of maladaptive thinking. The present study aimed to uncover interactions between childhood maltreatment and multiple genetic differences in irrational beliefs. Childhood maltreatment and irrational beliefs were assessed using multiple self-report instruments in a sample of healthy volunteers (N = 452). Eighteen single-nucleotide polymorphisms were genotyped in six candidate genes related to neurotransmitter function (COMT; SLC6A4; OXTR), neurotrophic factors (BDNF), and the hypothalamic-pituitary-adrenal axis (NR3C1; CRHR1). Gene-environment interactions (G×E) were first explored in models that employed one measure of childhood maltreatment and one measure of irrational beliefs. These effects were then followed up in models in which either the childhood maltreatment measure, the irrational belief measure, or both were substituted by parallel measures. Consistent results across models indicated that childhood maltreatment was positively associated with irrational beliefs, and these relations were significantly influenced by COMT rs165774 and OXTR rs53576. These results remain preliminary until independent replication, but they represent the best available evidence to date on G×E in a fundamental mechanism of psychopathology.

The effects of the interaction between polygenes and the parent-child relationship on junior high school students' aggressive behaviors were explored through the frameworks of gene-endophenotype-behavior and neurophysiological basis. A total of 892 junior high school students participated in this study. They were asked to complete self-reported questionnaires, and saliva samples were collected. Results showed that 5-HTTLPR, MAOA-uVNTR, COMT (rs4680), and Taq1 (rs1800497) of the DRD2 gene affected students' aggressive behaviors in an accumulative way. The polygenic risk score explained 3.4% of boys' aggression and 1.1% of girls' aggression. The interactions between polygenic risk score and parent-child conflict significantly affected the aggressive behaviors of male students, but did not show any significant effect on those of female students. The interactional effect of polygenic risk score and parent-child conflict on junior high school students' aggressive behaviors was completely mediated by frustration. However, the interaction effect of polygenic risk score and parent-child affinity on aggression was not affected by frustration. This study helps us better understand junior high school students' aggressive behaviors and promotes the prevention and correction of adolescents' problem behaviors.

The link between childhood maltreatment and mood disorders is complex and involves multiple bio-psycho-social factors that affect multiple molecular pathways. The present narrative review aims to clarify the current understanding of the impact of childhood maltreatment on biomarkers in patients with mood disorders and their first-degree relatives. Neurotransmitters, such as serotonin, dopamine, norepinephrine, and hormones (eg the stress hormone cortisol), play a crucial role in regulating mood and emotion. Childhood maltreatment can alter and affect the levels and functioning of these neurotransmitters in the brain; further, childhood maltreatment can lead to structural and connectivity changes in the brain, hence contributing to the development of mood disorders and moderating illness presentation and modifying response to treatments. Childhood maltreatment information, therefore, appears mandatory in treatment planning and is a critical factor in therapeutic algorithms. Further research is needed to fully understand these pathways and develop new treatment modalities for individuals with mood disorders who have experienced childhood maltreatment and effective preventive interventions for individuals at risk of developing mood disorders.

Debates about the concept of Free Will date back to ancient times. About 40 years ago, Benjamin Libet designed an experiment showing that the conscious intention to move is preceded by a specific pattern of brain activation. His finding suggested that unconscious processes determine our decisions. Libet-style experiments have continued to dominate the debate about Free Will, pushing some authors to argue that the existence of Free Will is a mere illusion. We believe that this dispute is because we often measure Free Will using arbitrary human decisions rather than deliberate actions. After reviewing the definition of Free Will and the related literature, we conclude that the scientific evidence does not disprove the existence of Free Will. However, our will encounters several constraints and limitations that should be considered when evaluating our deeds' personal responsibility.

Persson and Savulescu argue that moral bioenhancement is not only morally permissible; in some cases, it is morally obligatory. In this article, I introduce a new reason to worry about moral enhancement. I adapt the disability concept of misfit to show how moral enhancement could cause extreme moral disempowerment to those enhanced, which would result in moral injury. I argue that any safety framework that guides the development of moral bioenhancement must be sensitive to the problem of moral misfitting. I present the best case for moral bioenhancement before turning to my own worry concerning the development of moral bioenhancement and its practical implications. Finally, I consider a series of objections and responses.

The hypothalamus is key to body homeostasis, including regulating cortisol, testosterone, vasopressin, and oxytocin hormones, modulating aggressive behavior. Animal studies have linked the morphology and function of the hypothalamus to aggression and affiliation, with a subregional pattern reflecting the functional division between the hypothalamic nuclei. We explored the relationship between hypothalamic subunit volumes in violent offenders with (PSY-V) and without (NPV) a psychotic disorder, and the association with psychopathy traits. 3T MRI scans (n = 628, all male 18-70 years) were obtained from PSY-V, n = 38, NPV, n = 20, non-violent psychosis patients (PSY-NV), n = 134, and healthy controls (HC), n = 436. The total hypothalamus volume and its eleven nuclei were delineated into five subunits using Freesurfer v7.3. Psychopathy traits were assessed with Psychopathy Checklist-revised (PCL-R). ANCOVAs and linear regressions were used to analyze associations with subunit volumes. Both groups with a history of violence exhibited smaller anterior-superior subunit volumes than HC (NPV Cohen's d = 0.56, p = 0.01 and PSY-V d = 0.38, p = 0.01). There were no significant differences between HC and PSY-NV. PCL-R scores were positively associated with the inferior tubular subunit on a trend level (uncorrected p = 0.045, Cohen's d = 0.04). We found distinct hypothalamic subunit volume reductions in persons with a history of violence independent of concomitant psychotic disorder but not in persons with psychosis alone. The results provide further information about the involvement of the hypothalamus in aggression, which ultimately may lead to the development of targeted treatment for the clinical and societal challenge of aggression and violent behavior.

Congenital absence of monoamine oxidase A (MAO-A) activity predisposes to antisocial impulsive behaviour, and the MAOA uVNTR low-expressing genotype (MAOA-L) together with childhood maltreatment is associated with similar phenotypes in males. A possible explanation of how family environment may lead to such behaviour involves DNA methylation. We have assessed MAOA methylation and impulsive/antisocial behaviour in 121 males from the Estonian Children Personality Behaviour and Health Study. Of the 12 CpG sites measured, methylation levels at the locus designated CpG3 were significantly lower in subjects with antisocial behaviour involving police contact. CpG3 methylation was lower in subjects with alcohol use disorder by age 25, but only in MAOA-H genotype. No correlation between MAOA CpG3 methylation levels and adaptive impulsivity was found at age 15, but in MAOA-L genotype a positive correlation appeared by age 18. By age 25, this positive correlation was no longer observed in subjects with better family relationships but had increased further with experience of adversity within the family. MAOA CpG3 methylation had different developmental dynamics in relation to maladaptive impulsivity. At age 18, a positive correlation was observed in MAOA-L genotype with inferior family relationships and a negative correlation was found in MAOA-H with superior home environment; both of these associations had disappeared by age 25. CpG3 methylation was associated with dietary intake of several micronutrients, most notable was a negative correlation with the intake of zinc, but also with calcium, potassium and vitamin E; a positive correlation was found with intake of phosphorus. In conclusion, MAOA CpG3 methylation is related to both maladaptive and adaptive impulsivity in adolescence in MAOA-L males from adverse home environment. By young adulthood, this relationship with maladaptive impulsivity had disappeared but with adaptive impulsivity strengthened. Thus, MAOA CpG3 methylation may serve as a marker for adaptive developmental neuroplasticity in MAOA-L genotype. The mechanisms involved may include dietary factors.

Genetic polymorphism has been proven to have an important association with depression, which can influence the risk of developing depression, the efficacy of medications, and adverse effects via metabolic and neurological pathways. Nonetheless, aspects of the association between single nucleotide polymorphisms and depression have not been systematically investigated by bibliometric analysis.

The aim of this study was to analyze the current status and trends of single nucleotide polymorphism research on depression through bibliometric and visual analysis.

The Web of Science Core Collection was used to retrieve 10,043 articles that were published between 1998 and 2021. CiteSpace (6.1 R4) was used to perform collaborative network analysis, co-citation analysis, co-occurrence analysis, and citation burst detection.

The most productive and co-cited journals were the Journal of Affective Disorders and Biological Psychiatry, respectively, and an analysis of the references showed that the most recent research focused on the largest thematic cluster, "5-HT", reflecting the important research base in this area. "CYP2D6" has been in the spotlight since its emergence in 2009 and has become a research hotspot since its outbreak in 2019. However, "BDNF ", "COMT ", "older adults", "loci", and "DNA methylation" are also the new frontier of research, and some of them are currently in the process of exploration.

These findings offer a useful perspective on existing research and potential future approaches in the study of the association between single nucleotide polymorphisms and depression, which may assist researchers in selecting appropriate collaborators or journals.

To explain why individuals exposed to identical stressors experience divergent clinical outcomes, we determine how molecular encoding of stress modifies genetic risk for brain disorders. Analysis of post-mortem brain (n=304) revealed 8557 stress-interactive expression quantitative trait loci (eQTLs) that dysregulate expression of 915 eGenes in response to stress, and lie in stress-related transcription factor binding sites. Response to stress is robust across experimental paradigms: up to 50% of stress-interactive eGenes validate in glucocorticoid treated hiPSC-derived neurons (n=39 donors). Stress-interactive eGenes show brain region- and cell type-specificity, and, in post-mortem brain, implicate glial and endothelial mechanisms. Stress dysregulates long-term expression of disorder risk genes in a genotype-dependent manner; stress-interactive transcriptomic imputation uncovered 139 novel genes conferring brain disorder risk only in the context of traumatic stress. Molecular stress-encoding explains individualized responses to traumatic stress; incorporating trauma into genomic studies of brain disorders is likely to improve diagnosis, prognosis, and drug discovery.

Older brain age - as estimated from structural MRI data - is known to be associated with detrimental mental and physical health outcomes in older adults. Social isolation, which has similar detrimental effects on health, may be associated with accelerated brain aging though little is known about how different trajectories of social isolation across the life course moderate this association. We examined the associations between social isolation trajectories from age 5 to age 38 and brain age assessed at age 45.

We previously created a typology of social isolation based on onset during the life course and persistence into adulthood, using group-based trajectory analysis of longitudinal data from a New Zealand birth cohort. The typology comprises four groups: 'never-isolated', 'adult-only', 'child-only', and persistent 'child-adult' isolation. A brain age gap estimate (brainAGE) - the difference between predicted age from structural MRI date and chronological age - was derived at age 45. We undertook analyses of brainAGE with trajectory group as the predictor, adjusting for sex, family socio-economic status, and a range of familial and child-behavioral factors.

Older brain age in mid-adulthood was associated with trajectories of social isolation after adjustment for family and child confounders, particularly for the 'adult-only' group compared to the 'never-isolated' group.

Although our findings are associational, they indicate that preventing social isolation, particularly in mid-adulthood, may help to avert accelerated brain aging associated with negative health outcomes later in life.

Of late, internet addiction among adolescents has become a serious problem, with increased internet use. Previous research suggests that the more people become addicted to the internet, the more they isolate themselves from society. Conversely, it has been suggested that abundant social capital (the networks of relationships among people who live and work in a particular society) protects people from becoming addicted to the internet. This study focused on the brain structure of typical adolescents (10-18 years of age) and hypothesized that the size of the left dorsolateral prefrontal cortex (DLPFC), which is thought to be associated with self-control ability, is associated with both internet addiction and social capital. Voxel-based morphometry analysis indicated that left DLPFC volume was negatively correlated with the severity of internet addiction and positively correlated with social capital. Furthermore, correlation analysis demonstrated that the severity of internet addiction and social capital were negatively correlated. The statistical association between them was no longer significant when left DLPFC volume was used as a control variable. These results suggest that the left DLPFC may mediate the relationship between social capital and internet addiction in adolescents.

Objectives: Personality organization or functioning describes biographically acquired characteristics for the regulation of psychological processes. Limitations correlate with symptom load. This study examines whether significant improvement in personality functioning can be achieved in the framework of a multimodal psychodynamic treatment and its influence on the psychological symptoms. Methods: In this naturalistic study design (N = 318) personality organization was measured with the OPD-SQS and the symptoms were obtained using PHQ-9, GAD-7, SCL-9 and mini- Spin. Changes in the functioning levels were calculated using a t-test. The associations between the functional and symptom improvements were calculated using hierarchical regressionmodels. ANOVAs for dependent samples were used to calculate the association of the personality organization changes on symptom reduction Results: Treatment resulted in significant improvement in personality structure.The greater the changes, the lower the symptom burden at the end of treatment. Patients with lower personality structure benefited equally well from treatment. Conclusions: Personality functioning improves with multimodal psychodynamic therapy and is accompanied by reduction of psychological symptoms. Structural changes proceed equally in high and low structured patients.

Aggression is a complex social behavior, critically involving brain serotonin (5-HT) function. The neurobiology of female aggression remains elusive, while the incidence of its manifestations has been increasing. Yet, animal models of female aggression are scarce. We previously proposed a paradigm of female aggression in the context of gene x environment interaction where mice with partial genetic inactivation of tryptophan hydroxylase-2 (Tph2+/- mice), a key enzyme of neuronal 5-HT synthesis, are subjected to predation stress resulting in pathological aggression. Using deep sequencing and the EBSeq method, we studied the transcriptomic signature of excessive aggression in the prefrontal cortex of female Tph2+/- mice subjected to rat exposure stress and food deprivation. Challenged mutants, but not other groups, displayed marked aggressive behaviors. We found 26 genes with altered expression in the opposite direction between stressed groups of both Tph2 genotypes. We identified several molecular markers, including Dgkh, Arfgef3, Kcnh7, Grin2a, Tenm1 and Epha6, implicated in neurodevelopmental deficits and psychiatric conditions featuring impaired cognition and emotional dysregulation. Moreover, while 17 regulons, including several relevant to neural plasticity and function, were significantly altered in stressed mutants, no alteration in regulons was detected in stressed wildtype mice. An interplay of the uncovered pathways likely mediates partial Tph2 inactivation in interaction with severe stress experience, thus resulting in excessive female aggression.

Evolutionary genetics has long struggled with understanding how functional genes under selection remain polymorphic in natural populations. Taking as a starting point that natural selection is ultimately a manifestation of ecological processes, we spotlight an underemphasized and potentially ubiquitous ecological effect that may have fundamental effects on the maintenance of genetic variation. Negative frequency dependency is a well-established emergent property of density dependence in ecology, because the relative profitability of different modes of exploiting or utilizing limiting resources tends to be inversely proportional to their frequency in a population. We suggest that this may often generate negative frequency-dependent selection (NFDS) on major effect loci that affect rate-dependent physiological processes, such as metabolic rate, that are phenotypically manifested as polymorphism in pace-of-life syndromes. When such a locus under NFDS shows stable intermediate frequency polymorphism, this should generate epistatic selection potentially involving large numbers of loci with more minor effects on life-history (LH) traits. When alternative alleles at such loci show sign epistasis with a major effect locus, this associative NFDS will promote the maintenance of polygenic variation in LH genes. We provide examples of the kind of major effect loci that could be involved and suggest empirical avenues that may better inform us on the importance and reach of this process.