Neuroscience research underscores the critical impact of adverse experiences on brain development. Yet, there is limited understanding of the specific pathways linking adverse experiences to accelerated or delayed brain development and their ultimate contributions to psychopathology. Here, we present new longitudinal data demonstrating that neurocognitive functioning during adolescence, as affected by adverse experiences, predicts psychopathology during young adulthood. The sample included 167 participants (52% male) assessed in adolescence and young adulthood. Adverse experiences were measured by early maltreatment experiences and low family socioeconomic status. Cognitive control was assessed by neural activation and behavioral performance during the Multi-Source Interference Task. Psychopathology was measured by self-reported internalizing and externalizing symptomatology. Results indicated that higher maltreatment predicted heightened frontoparietal activation during cognitive control, indicating delayed neurodevelopment, which, in turn predicted higher internalizing and externalizing symptomatology. Furthermore, higher maltreatment predicted a steeper decline in frontoparietal activation across adolescence, indicating neural plasticity in cognitive control-related brain development, which was associated with lower internalizing symptomatology. Our results elucidate the crucial role of neurocognitive development in the processes linking adverse experiences and psychopathology. Implications of the findings and directions for future research on the effects of adverse experiences on brain development are discussed.

Conduct disorder (CD), characterized by youth antisocial behavior, is associated with a variety of neurocognitive impairments. However, questions remain regarding the neural underpinnings of these impairments. To investigate novel neural mechanisms that may support these neurocognitive abnormalities, the present study applied a graph analysis to resting-state functional magnetic resonance imaging (fMRI) data collected from a national sample of 4,781 youth, ages 9–10, who participated in the baseline session of the Adolescent Brain Cognitive DevelopmentSM Study (ABCD Study®). Analyses were then conducted to examine the relationships among levels of CD symptomatology, metrics of global topology, node-level metrics for subcortical structures, and performance on neurocognitive assessments. Youth higher on CD displayed higher global clustering (β = .039, 95% CIcorrected [.0027 .0771]), but lower Degreesubcortical (β = −.052, 95% CIcorrected [−.0916 −.0152]). Youth higher on CD had worse performance on a general neurocognitive assessment (β = −.104, 95% CI [−.1328 −.0763]) and an emotion recognition memory assessment (β = −.061, 95% CI [−.0919 −.0290]). Finally, global clustering mediated the relationship between CD and general neurocognitive functioning (indirect β = −.002, 95% CI [−.0044 −.0002]), and Degreesubcortical mediated the relationship between CD and emotion recognition memory performance (indirect β = −.002, 95% CI [−.0046 −.0005]). CD appears associated with neuro-topological abnormalities and these abnormalities may represent neural mechanisms supporting CD-related neurocognitive disruptions.

Theoretical models of attention-deficit/hyperactivity disorder implicate neurocognitive dysfunction, yet neurocognitive functioning covers a range of abilities that may not all be linked with inattention. This study (a) investigated the single nucleotide polymorphism (SNP) heritability (h2SNP) of inattention and aspects of neurocognitive efficiency (memory, social cognition, executive function, and complex cognition) based on additive genome-wide effects; (b) examined if there were shared genetic effects among inattention and each aspect of neurocognitive efficiency; and (c) conducted an exploratory genome-wide association study to identify genetic regions associated with inattention. The sample included 3,563 participants of the Philadelphia Neurodevelopmental Cohort, a general population sample aged 8–21 years who completed the Penn Neurocognitive Battery. Data on inattention was obtained with the Kiddie Schedule of Affective Disorders (adapted). Genomic relatedness matrix restricted maximum likelihood was implemented in genome-wide complex trait analysis. Analyses revealed significant h2SNP for inattention (20%, SE = 0.08), social cognition (13%, SE = 0.08), memory (17%, SE = 0.08), executive function (25%, SE = 0.08), and complex cognition (24%, SE = 0.08). There was a positive genetic correlation (0.67, SE = 0.37) and a negative residual covariance (−0.23, SE = 0.06) between inattention and social cognition. No SNPs reached genome-wide significance for inattention. Results suggest specificity in genetic overlap among inattention and different aspects of neurocognitive efficiency.

This study evaluated associations between pre-deployment neurocognitive performance and post-deployment posttraumatic stress disorder (PTSD) symptoms in a sample of deployed active duty Army soldiers. As part of a larger longitudinal study, each participant completed baseline measures of memory, executive attention, and response inhibition, and baseline and post-deployment self-report measures of PTSD symptom severity. Data were subjected to multiple regression analyses that examined associations between baseline neurocognitive performances and longitudinal PTSD symptom outcome. Results revealed that pre-trauma immediate recall of visual information was associated with post-deployment PTSD symptom severity, even after controlling for pre-deployment PTSD symptom levels, combat intensity, age, gender, and test-retest interval. There was also an interaction between pre-deployment PTSD symptom severity and pre-deployment immediate visual recall and verbal learning, indicating that neurocognitive performances were more strongly (and negatively) associated with residualized post-deployment PTSD symptoms at higher levels of pre-deployment PTSD symptoms. These findings highlight the potential role of pre-trauma neurocognitive functioning in moderating the effects of trauma exposure on PTSD symptoms.(JINS, 2009, 15, 840–852.)

The relationship between MRI findings (i.e., subcortical hyperintensities; SH, whole brain volume) and the cognitive dysfunction of vascular dementia (VaD) was examined. Participants included 24 persons that met NINDS-AIREN criteria for VaD (MMSE = 19.9 ± 4.2) and underwent comprehensive neuropsychological assessment and MRI brain imaging. The volume of subcortical hyperintensities (SH) was strongly associated with executive–psychomotor performance, but not with performance across other cognitive domains or global cognitive functional level. Conversely, WBV was strongly associated with global cognitive functioning and performance across most cognitive domains (memory, language, visual integration), but not with executive–psychomotor functioning. The failure of SH to account for either the global dementia evident in these VaD patients or impairments across most cognitive domains suggests that deep subcortical white matter disease may only indirectly contribute to the global cognitive dysfunction of VaD. That WBV emerged as a stronger correlate of dementia raises further questions regarding the cerebral mechanisms that contribute to the development of VaD. (JINS, 2002, 8, 743–752.)