The age at which a parent has a child impacts the child's cognition and risk for mental illness. It appears that this risk is curvilinear, with both age extremes associated with lower intelligence and increased prevalence of some neuropsychiatric disorders. Little is known of the neural mechanisms underpinning this phenomenon. We extracted lobar volumes, surface areas, and cortical thickness from 489 neuroanatomic magnetic resonance images acquired on 171 youth. Using linear mixed model regression, we determined the association between parental age and offspring's neuroanatomy, adjusting for offspring's age, sex, intelligence, and parental socioeconomic class. For gray matter volumes, quadratic paternal and maternal age terms contributed significantly (maternal quadratic age effect: t = -2.2, P = 0.03; paternal quadratic age effect: t = -2.4, P = 0.02) delineating an inverted "U" relationship between parental age and gray matter volume. Cortical volume increased with both advancing paternal and maternal age until around the early 30s after which it fell. Paternal age effects were more pronounced on cortical surface area, whereas maternal age impacted more on cortical thickness. There were no significant effects of parental age on white matter volumes. These parental age effects on cerebral morphology may form part of the link between parental age extremes and suboptimal neurocognitive outcomes.
Objective: There is considerable epidemiological and neuropsychological evidence that attention deficit hyperactivity disorder (ADHD) is best considered dimensionally, lying at the extreme end of a continuous distribution of symptoms and underlying cognitive impairments. The authors investigated whether cortical brain development in typically developing children with symptoms of hyperactivity and impulsivity resembles that found in the syndrome of ADHD. Specifically, they examined whether a slower rate of cortical thinning during late childhood and adolescence, which they previously found in ADHD, is also linked to the severity of symptoms of hyperactivity and impulsivity in typically developing children. Method: In a longitudinal analysis, a total of 193 typically developing children with 389 neuroanatomic magnetic resonance images and varying levels of symptoms of hyperactivity and impulsivity (measured with the Conners' Parent Rating Scale) were contrasted with 197 children with ADHD with 337 imaging scans. The relationship between the rates of regional cortical thinning and severity of symptoms of hyperactivity/impulsivity was determined. Results: Youth with higher levels of hyperactivity/impulsivity had a slower rate of cortical thinning, predominantly in prefrontal cortical regions, bilaterally in the middle frontal/premotor gyri, extending down the medial prefrontal wall to the anterior cingulate; the orbitofrontal cortex; and the right inferior frontal gyrus. For each increase of one point in the hyperactivity/impulsivity score, there was a decrease in the rate of regional cortical thinning of 0.0054 mm/year (SE=0.0019 mm/year). Children with ADHD had the slowest rate of cortical thinning. Conclusions: Slower cortical thinning during adolescence characterizes the presence of both the symptoms and syndrome of ADHD, providing neurobiological evidence for dimensionality of the disorder.
The purpose of the present study was to advance our understanding of neurobiological processes related to the intergenerational transmission of behavior problems related to emotional dysregulation by examining whether earlier and/or more chronic exposure to maternal depression would be associated with increased depressive symptoms and reactive aggressive behaviors in young adult offspring, and whether individual differences in amygdala volume, hippocampal volume, and/or amygdala:hippocampus volume ratio would mediate this association. Results were mixed, indicating that maternal depression evident in early childhood or chronic maternal depression was positively associated with offspring depression and reactive aggression in early adulthood in some but not all cases. Maternal depression was not significantly associated with the volume of any individual brain regions in offspring, but was, in some analyses, significantly associated with larger amygdala:hippocampal volume ratios. Likewise, the volume of individual brain regions was not linked with concurrent young adult depression or reactive aggression, but amygdala:hippocampal volume ratio was linked to young adult reactive aggression. Results did not support a mediating role for any individual brain region in the associations found between maternal depression and offspring depression or reactive aggression, but did suggest a mediating role for offspring amygdala:hippocampal volume ratio in the association between maternal depression trajectory grouping and offspring reactive aggression in young adulthood. Findings support a role for relative amygdala and hippocampus size in the intergenerational transmission of problems related to emotion regulation.
Using a cohort of 310 low‐income male adolescents living in an urban community and followed prospectively from 18 months through adolescence (ages 15–18 years), the current study examined whether individual, family, and community risk factors from ages 18 to 42 months were associated with adolescents' violent behavior, as indexed by juvenile petitions. Results of multivariate analyses indicated that although family income was the only factor to discriminate those with no arrest record from those with nonviolent arrests, rejecting parenting, child oppositional behavior, emotion regulation, and minority status during the toddler period contributed unique variance in distinguishing male adolescents arrested for violent behavior compared to those never arrested and those arrested for nonviolent behavior. Implications for prevention efforts are discussed.
Background There is abundant evidence that offspring of depressed mothers are at increased risk for persistent behavior problems related to emotion regulation, but the mechanisms by which offspring incur this risk are not entirely clear. Early adverse caregiving experiences have been associated with structural alterations in the amygdala and hippocampus, which parallel findings of cortical regions altered in adults with behavior problems related to emotion regulation. This study examined whether exposure to maternal depression during childhood might predict increased aggression and/or depression in early adulthood, and whether offspring amygdala:hippocampal volume ratio might mediate this relationship. Methods Participants were 258 mothers and sons at socioeconomic risk for behavior problems. Sons' trajectories of exposure to maternal depression were generated from eight reports collected prospectively from offspring ages 18 months to 10 years. Offspring brain structure, aggression, and depression were assessed at age 20 ( n = 170). Results Persistent, moderately high trajectories of maternal depression during childhood predicted increased aggression in adult offspring. In contrast, stable and very elevated trajectories of maternal depression during childhood predicted depression in adult offspring. Increased amygdala: hippocampal volume ratios at age 20 were significantly associated with concurrently increased aggression, but not depression, in adult offspring. Offspring amygdala: hippocampal volume ratio mediated the relationship found between trajectories of moderately elevated maternal depression during childhood and aggression in adult offspring. Conclusions Alterations in the relative size of brain structures implicated in emotion regulation may be one mechanism by which offspring of depressed mothers incur increased risk for the development of aggression.
Guided by a bridging model of pathways leading to low-income boys' early starting and persistent trajectories of antisocial behavior, the current article reviews evidence supporting the model from early childhood through early adulthood. Using primarily a cohort of 310 low-income boys of families recruited from Women, Infants, and Children Nutrition Supplement centers in a large metropolitan area followed from infancy to early adulthood and a smaller cohort of boys and girls followed through early childhood, we provide evidence supporting the critical role of parenting, maternal depression, and other proximal family risk factors in early childhood that are prospectively linked to trajectories of parent-reported conduct problems in early and middle childhood, youth-reported antisocial behavior during adolescence and early adulthood, and court-reported violent offending in adolescence. The findings are discussed in terms of the need to identify at-risk boys in early childhood and methods and platforms for engaging families in healthcare settings not previously used to implement preventive mental health services.
