Background Individuals with autism spectrum disorders (ASD) often exhibit symptoms of Attention-Deficit/Hyperactivity Disorder (ADHD). Across both disorders, observations of distributed functional abnormalities suggest aberrant large-scale brain network connectivity. Yet, common and distinct network correlates of ASD and ADHD remain unidentified. Here, we aimed to examine patterns of dysconnection in school-age children with ASD, ADHD and typically developing children (TDC) who completed a resting state fMRI (R-fMRI) scan. Methods We measured voxel-wise network centrality, functional connectivity metrics indexing local (degree centrality; DC) and global (eigenvector centrality; EC) functional relationships across the entire brain connectome, in R-fMRI data from 56 children with ASD, 45 children with ADHD and 50 TDC. A one-way ANCOVA, with group as fixed factor (whole-brain corrected), was followed by post-hoc pair-wise comparisons. Results Cortical and subcortical areas exhibited centrality abnormalities; some common to both ADHD and ASD, such as in precuneus. Others were disorder-specific and included ADHD-related increases in DC in right striatum/pallidum, in contrast with ASD-related increases in bilateral temporolimbic areas. Secondary analyses differentiating children with ASD into those with or without ADHD-like comorbidity (ASD+ and ASD−, respectively) revealed that the ASD+ group shared ADHD-specific abnormalities in basal ganglia. By contrast, centrality increases in temporolimbic areas characterized children with ASD regardless of ADHD-like comorbidity. At the cluster level eignevector centrality group patterns were similar to DC. Conclusions ADHD and ASD are neurodevelopmental disorders with distinct and overlapping clinical presentations. This work provides evidence for both shared and distinct underlying mechanisms at the large-scale network level.
The debilitating nature of schizophrenia necessitates early detection of individuals at clinical high-risk (CHR) in order to facilitate early intervention. In particular, comparisons between those who develop fully psychotic features (CHR+) and those who do not (CHR−) offer the opportunity to reveal distinct risk factors for psychosis, as well as possible intervention target points. Recent studies have investigated baseline clinical, neurocognitive, neuroanatomic, neurohormonal, and psychophysiological predictors of outcome; premorbid social dysfunction, deficits in neurocognitive performance, neuroanatomic changes, and hypothalamic-pituitary-adrenal (HPA) axis dysfunction have been implicated in psychosis emergence. However, several challenges within CHR research remain: heterogeneity in long-term diagnostic outcome, the variability of research tools and definitions utilized, and limited longitudinal follow-up. Future work in the field should focus on replication via extended longitudinal designs, aim to explore the trajectories and inter-relationships of hypothesized biomarkers, and continue to investigate interventions that seek to prevent psychosis emergence through symptom reduction.
Schizophrenia is a devastating mental illness afflicting about 1 percent of the population, involving delusions and hallucinations. Although originally believed to be a disorder of neurodegeneration, multiple lines of inquiry now provide compelling evidence for its neurodevelopmental origins. As such, one of the most puzzling aspects about this disorder is its characteristic onset in late adolescence or early adulthood. In this chapter we review evidence for the involvement of both early (genetic and perinatal) and later (adolescent) neurodevelopmental influences in the etiology and pathogenesis of schizophrenia. New findings regarding its genetic architecture implicate both common and rare genetic variants that converge on pathways involving disruption of synaptic plasticity, which may be related to neural endophenotypes present in both patients and their clinically unaffected relatives. Together, these findings suggest a combination of these early and later neurodevelopmental factors converge to produce the cellular, structural, and functional deficits underlying the disorder.
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