Attention deficit hyperactive disorder (ADHD) and Autism spectrum disorders (ASD) are two of the most common and vexing neurodevelopmental disorders among children. Although the two disorders share many behavioral and neuropsychological characteristics, most MRI studies examine only one of the disorders at a time. Using graph theory combined with structural and functional connectivity, we examined the large-scale network organization among three groups of children: a group with ADHD (8-12 years, n = 20), a group with ASD (7-13 years, n = 16), and typically developing controls (TD) (8-12 years, n = 20). We apply the concept of the rich-club organization, whereby central, highly connected hub regions are also highly connected to themselves. We examine the brain into two different network domains: (1) inside a rich-club network phenomena, and (2) outside a rich-club network phenomena. ASD and ADHD populations had markedly different patterns of rich club and non rich-club connections in both functional and structural data. The ASD group exhibited higher connectivity in structural and functional networks but only inside the rich-club networks. These findings were replicated using the autism brain imaging data exchange (ABIDE) dataset with ASD (n = 85) and TD (n = 101). The ADHD group exhibited a lower generalized fractional anisotropy (GFA) and functional connectivity inside the rich-club networks, but a higher number of axonal fibers and correlation coefficient values outside the rich-club. Despite some shared biological features and frequent comorbity, these data suggest ADHD and ASD exhibit distinct large-scale connectivity patterns in middle childhood.

Interest in the value of Omega—3 (n—3) fatty acid supplementation for treatment of ADHD remains high. No prior meta-analysis has examined whether ADHD is associated with alterations in blood lipid levels and meta-analyses of supplementation have reached conflicting conclusions. Methods We report two new meta-analyses. Study 1 examined blood levels of Omega—3 fatty acids in relation to ADHD. Study 2 examined a larger sample of randomized intervention trials than previously reported. Results Study 1 included 9 studies (n = 586) and found lower overall blood levels of n—3 in individuals with ADHD versus controls (g = 0.42, 95% CI = 0.26–0.59; p < .001). Study 2 included 16 studies (n = 1408) and found that n—3 supplementation improved ADHD composite symptoms; using the best available rating and reporter (g = 0.26, 95% CI = 0.15–0.37; p < .001). Supplementation showed reliable effects on hyperactivity by parent and teacher report, but reliable effects for inattention only by parent report. Conclusions Omega—3 levels are reduced in children with ADHD. Dietary supplementation appears to create modest improvements in symptoms. There is sufficient evidence to consider Omega—3 fatty acids as a possible supplement to established therapies. However it remains unclear whether such intervention should be confined to children with below normal blood levels.

Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are commonly comorbid, share genetic liability, and often exhibit overlapping cognitive impairments. Clarification of shared and distinct cognitive effects while considering comorbid symptoms across disorders has been lacking. In the current study, children ages 7-15 years assigned to three diagnostic groups:ADHD (n = 509), ASD (n = 97), and controls (n = 301) completed measures spanning the cognitive domains of attention/arousal, working memory, set-shifting, inhibition, and response variability. Specific processes contributing to response variability were examined using a drift diffusion model, which separately quantified drift rate (i.e., efficiency of information processing), boundary separation (i.e., speed-accuracy trade-offs), and non-decision time. Children with ADHD and ASD were impaired on attention/arousal, processing speed, working memory, and response inhibition, but did not differ from controls on measures of delayed reward discounting, set-shifting, or interference control. Overall, impairments in the ASD group were not attributable to ADHD symptoms using either continuous symptom measures or latent categorical grouping approaches. Similarly, impairments in the ADHD group were not attributable to ASD symptoms. When specific RT parameters were considered, children with ADHD and ASD shared impairments in drift rate. However, children with ASD were uniquely characterized by a wider boundary separation. Findings suggest a combination of overlapping and unique patterns of cognitive impairment for children with ASD as compared to those with ADHD, particularly when the processes underlying reaction time measures are considered separately.

Background To determine whether familial transmission is shared between autism spectrum disorders and attention-deficit/hyperactivity disorder, we assessed the prevalence, rates of comorbidity, and familial transmission of both disorders in a large population-based sample of children during a recent seven year period. Methods Study participants included all children born to parents with the Kaiser Permanente Northwest (KPNW) Health Plan between January 1, 1998 and December 31, 2004 (n = 35,073). Children and mothers with physician-identified autism spectrum disorders (ASD) and/or attention-deficit/hyperactivity disorder (ADHD) were identified via electronic medical records maintained for all KPNW members. Results Among children aged 6-12 years, prevalence was 2.0% for ADHD and 0.8% for ASD; within those groups, 0.2% of the full sample (19% of the ASD sample and 9.6% of the ADHD sample) had co-occurring ASD and ADHD, when all children were included. When mothers had a diagnosis of ADHD, first born offspring were at 6-fold risk of ADHD alone (OR=5.02, p<0.0001) and at 2.5-fold risk of ASD alone (OR=2.52, p<0.01). Results were not accounted for by maternal age, child gestational age, child gender, and child race. Conclusions ASD shares familial transmission with ADHD. ADHD and ASD have a partially overlapping diathesis.

Depression in adults is associated with deficits in a number of cognitive domains, however it remains less clear how early in development theses deficits can be detected in early onset depression. There are several different hypotheses about the links between cognitive function and depression. For example, it has been argued that executive function deficits contribute to emotion regulation difficulties, which in turn increase risk for depression. Further, it has been suggested that some cognitive deficits, such as episodic memory, may reflect hippocampal abnormalities linked to both depression and episodic memory. We examined these questions in adolescents participating in a longitudinal study of preschool onset depression. We measured cognitive function at adolescence using the NIH toolbox (vocabulary, processing speed, executive function, working memory and episodic memory), and examined relationships of cognitive deficits to depression, emotion regulation, life stress and adversity, as well as hippocampal volume trajectories over three imaging assessments starting at school age. Depression related deficits in episodic memory were found. Youths with either current and past depression showed episodic memory deficits even after controlling for other psychopathology and family income. Depression severity, emotion dysregulation and life stress/adversity all predicted episodic memory impairment, as did smaller intercepts and slopes of hippocampal growth over time. Modest relationships of depression to hippocampal volume and strong relationships between emotion regulation and both episodic memory and hippocampal volume were found. These data are consistent with prior work in adults linking depression, episodic memory, emotion regulation, life stress/adversity and hippocampal volume in adults and suggest similar relations are evident as early as adolescence when memory systems are under development.