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Objective: To examine whether putatively atypical neuronal activity during internal attention in ADHD yields insights into processes underlying emotion dysregulation. Methods: We used a word processing paradigm to assess neural activations in adults with ADHD ( N = 46) compared to controls ( N = 43). We measured effects of valence, applied partial-least squares correlation analysis to assess multivariate brainbehavior relationships and ran subgroup analyses to isolate results driven by pure ADHD ( N = 18). Results: During internal attention, ADHD, compared to controls, have (1) increased activation in the right angular gyrus (rAG), which appears driven by pure, not comorbid, ADHD and (2) diminished activation in the insula and fronto-striatal circuitry. Diminished activations were driven by negatively-valenced internal attention and negatively correlated with increased affective lability within the ADHD group. Conclusion: Internal attention in ADHD is associated with increased rAG activation, possibly reflecting difficulty converging external and internal information, and diminished activation within emotion regulation circuitry.

Introduction: There has been no study in the literature evaluating serum tumor necrosis factor-like weak inducer of apoptosis (TWEAK) levels in attention-deficit/hyperactivity disorder (ADHD). Therefore, we performed the present study to specifically measure serum TWEAK levels to see whether or not its eventual alterations might have an etiopathogenetic significance in children with ADHD. Subjects and methods: A total of 49 treatment-naive children with ADHD and 39 healthy controls were included in the present study. The severities of ADHD and conduct disorder symptoms were assessed via parent- and teacher-rated questionnaires. Venous blood samples were collected, and serum TWEAK levels were measured. Results: Serum TWEAK levels of the ADHD group were significantly lower than the control group. Conclusions: This study shows that ADHD patients have decreased serum TWEAK levels, suggesting a possible involvement of TWEAK in the etiopathogenesis of ADHD.

Objective: Among screen-addicted children, there is a risk of insulin resistance (IR), obesity, hypertriglyceridemia and diabetes mellitus type 2 due to decreased physical activity and irregular eating habits. Most recently, relations of screen addiction (SA) and attention-deficit hyperactivity disorder (ADHD) with obesity have been reported. Herein, we aimed to investigate the presence of IR and dependent factors in screen-addicted children with and without obesity. Method: A total of 108 children in the age range of 11-17 years were included in the study. Cases were divided into three groups according to ADHD and SA scale scores. In these three groups, there were equal numbers of obese and non-obese patients. Homeostasis model assessment for insulin resistance (HOMA-IR) of the patients was assessed at baseline. Body fat analysis was performed with TANITA BC-420 MA body composition analyzers. All cases wore pedometers for 3 days to determine their basal metabolic rates (BMR) during active and sedentary periods. Carbohydrate, fat and calorie consumption was calculated using a professional nutrition program. Results: There were no statistically significant differences between the SA and non-SA groups on the energy consumption, BMR and fat mass and dietary contents. There was no effect of ADHD and SA on HOMA-IR values. Conclusion: We did not find any association between SA and IR. Also dependent factors were similar between groups. New studies are needed to determine how SA affects obesity., Ege University Scientific Research Projects (EGEBAP) [2013-TIP-017], This project was supported by Ege University Scientific Research Projects (EGEBAP) with grant number 2013-TIP-017.

ObjectiveThis study investigated the effects of a school-based skill-training intervention in attention control and executive functions for pupils with hyperactivity-impulsivity (H-I) and cognitive control (CC) deficits. The main aim was to examine whether the intervention differently influenced H-I and CC, and whether cognitive abilities or conduct problems moderated response to the intervention.MethodElementary school pupils from 41 schools participated the study and were divided into an intervention group (n = 71) and a waitlist control group (n = 77). Intervention outcomes were assessed with an inventory assessing executive function difficulties (including H-I and CC) completed by classroom teachers.ResultsSignificant intervention effects and positive changes were detected in CC but not in H-I. Significant intervention effects were found mainly among pupils with low levels of conduct problems.ConclusionsThe results suggest that a skill-training intervention has specific positive effects on CC, but conduct problems may diminish response to intervention.

Analyses of the polygenic architecture of childhood, persistent and late-diagnosed attention-deficit hyperactivity disorder (ADHD) in a Danish population-based case-cohort sample identify differences among ADHD subgroups with respect to common and rare variants. Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with onset in childhood (childhood ADHD); two-thirds of affected individuals continue to have ADHD in adulthood (persistent ADHD), and sometimes ADHD is diagnosed in adulthood (late-diagnosed ADHD). We evaluated genetic differences among childhood (n = 14,878), persistent (n = 1,473) and late-diagnosed (n = 6,961) ADHD cases alongside 38,303 controls, and rare variant differences in 7,650 ADHD cases and 8,649 controls. We identified four genome-wide significant loci for childhood ADHD and one for late-diagnosed ADHD. We found increased polygenic scores for ADHD in persistent ADHD compared with the other two groups. Childhood ADHD had higher genetic overlap with hyperactivity and autism compared with late-diagnosed ADHD and the highest burden of rare protein-truncating variants in evolutionarily constrained genes. Late-diagnosed ADHD had a larger genetic overlap with depression than childhood ADHD and no increased burden in rare protein-truncating variants. Overall, these results suggest a genetic influence on age at first ADHD diagnosis, persistence of ADHD and the different comorbidity patterns among the groups.

Background: Epidemiological studies suggest a link between eczema and attention deficit hyperactivity disorder (ADHD), but underlying mechanisms have not been examined. Objective: We aim to investigate the association between eczema and subsequent ADHD symptoms in the Growing Up in Singapore Towards healthy Outcomes cohort and explore the role of pro-inflammatory cytokines and gut microbiome. Methods: The modified International Study of Asthma and Allergies in Childhood questionnaire and Computerized Diagnostic Interview Schedule for Children Version IV were administered to assess reported eczema within the first 18 months and presence of ADHD symptoms at 54 months, respectively. Skin prick testing at 18 months, cytokines in maternal blood during pregnancy and cord blood and the mediating role of the gut microbiome at 24 months were assessed. Results: After adjusting for confounders, eczema with or without a positive skin prick test was associated with doubling the risk of ADHD symptoms. No differences in maternal and cord blood cytokines were observed in children with and without eczema, or children with and without ADHD. Gut microbiome dysbiosis was observed in children with eczema and children with ADHD. Children with eczema also had lower gut bacterial Shannon diversity. However, the relationship between eczema and ADHD was not mediated by gut microbiome. Conclusion: Early life eczema diagnosis is associated with a higher risk of subsequent ADHD symptoms in children. We found no evidence for underlying inflammatory mechanism or mediation by gut microbiome dysbiosis. Further research should evaluate other mechanisms underlying the link between eczema and ADHD. Clinical Trial Registration: [https://clinicaltrials.gov/ct2/show/NCT01174875], identifier [NCT01174875]. Ministry of Health (MOH) National Medical Research Council (NMRC) National Research Foundation (NRF) Published version This work was supported by the Singapore National Research Foundation under its Translational and Clinical Research (TCR) Flagship Programme and administered by the Singapore Ministry of Health’s National Medical Research Council (NMRC), Singapore-NMRC/TCR/004-NUS/2008; NMRC/TCR/012- NUHS/2014. ET was supported by the National Medical Research Council (NMRC) Transition Award grant [MOH-TA18nov003] from NMRC, Singapore.

Contains fulltext : 287469.pdf (Publisher’s version ) (Open Access) Attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are highly heritable neurodevelopmental conditions, with considerable overlap in their genetic etiology. We dissected their shared and distinct genetic etiology by cross-disorder analyses of large datasets. We identified seven loci shared by the disorders and five loci differentiating them. All five differentiating loci showed opposite allelic directions in the two disorders and significant associations with other traits, including educational attainment, neuroticism and regional brain volume. Integration with brain transcriptome data enabled us to identify and prioritize several significantly associated genes. The shared genomic fraction contributing to both disorders was strongly correlated with other psychiatric phenotypes, whereas the differentiating portion was correlated most strongly with cognitive traits. Additional analyses revealed that individuals diagnosed with both ASD and ADHD were double-loaded with genetic predispositions for both disorders and showed distinctive patterns of genetic association with other traits compared with the ASD-only and ADHD-only subgroups. These results provide insights into the biological foundation of the development of one or both conditions and of the factors driving psychopathology discriminatively toward either ADHD or ASD.

Objectives Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disorder and Sluggish Cognitive Tempo (SCT) might be a second inattention disorder that might be even affected by different attention pathways. SCT is characterized by daydreaming, mental confusion, staring blankly and hypoactivity. In the present study, we evaluated 5 common variants (rs6265, rs3746544, rs1051312, rs133946 and rs133945) located in 3 candidate genes (BDNF, SNAP25 and SYN III) that are known to take part in synaptic plasticity and neurotransmitter transmission. Methods We tested the effects of these variants on neuropsychological findings assessed by a computer-based neuropsychological test battery in children with inattention symptoms (SCT and/or ADHD). Results BDNF (rs6265), SNAP25 (rs3746544 and rs1051312) and SYN III (rs133946 and rs133945) polymorphisms were associated with variable cognitive measures. BDNF gene (rs6265) polymorphism Met allele carriers and SNAP25 gene (rs3746544) T allele carriers had an association with the attention domain. SNAP25 gene (rs1051312) C allele carriers were only associated with reaction time scores. Cognitive flexibility, which is one of the key components of executive function evaluation and shifting attention test scores were associated with BDNF (rs6265) Met allele and SYN III (rs133946) gene G allele. SYN III (rs133945) gene C allele carriers had an association with verbal memory correct hit scores. Conclusions As a conclusion, BDNF, SNAP25 and SYN III genes were associated with specific neurocognitive outcomes in children with inattention symptoms. It is important to note that exploring genotyping effects on neurocognitive functions instead of a heterogeneous psychiatric diagnosis can improve our understanding of psychopathologies., Ege University [TTU-2018-20009], This study was supported by the Ege University Scientific Research Projects Coordinator [TTU-2018-20009].

Attention-deficit/hyperactivity disorder (ADHD) in adults is understudied, especially regarding neural mechanisms such as oscillatory control of attention sampling. We report an electroencephalography (EEG) study of such cortical mechanisms, in ADHD-diagnosed adults during administration of Test of Variables of Attention (TOVA), a gold-standard continuous performance test for ADHD that measures the ability to sustain attention and inhibit impulsivity. We recorded 53 adults (28 female, 25 male, aged 18-60), and 18 matched healthy controls, using 128-channel EEG. We analyzed sensor-space features established as neural correlates of attention: timing-sensitivity and phase-synchrony of response activations, and event-related (de)synchronization (ERS/D) of alpha and theta frequency band activity; in frontal and parietal scalp regions. TOVA test performance significantly distinguished ADHD adults from neurotypical controls, in commission errors, response time variability (RTV) and d' (response sensitivity). The ADHD group showed significantly weaker target-locked and responselocked amplitudes, that were strongly right-lateralized at the N2 wave, and weaker phase synchrony (longer reset poststimulus). They also manifested significantly less parietal prestimulus 8-Hz theta ERS, less frontal and parietal poststimulus 4-Hz theta ERS, and more frontal and parietal prestimulus alpha ERS during correct trials. These differences may reflect excessive modulation of endogenous activity by strong entrainment to stimulus (alpha), combined with deficient modulation by neural entrainment to task (theta), which in TOVA involves monitoring stimulus spatial location (not predicted occurrence onset which is regular and task-irrelevant). Building on the hypotheses of theta coding for relational structure and rhythmic attention sampling, our results suggest that ADHD adults have impaired attention sampling in relational categorization tasks.

Background Attention-deficit/hyperactivity disorder (ADHD) is associated with negative life outcomes and recent studies have linked it to increased mortality. These studies have examined nationwide registers or clinic-referred samples and mostly included participants up until the age of 30. No studies have investigated mortality associated with subthreshold levels of ADHD symptoms. Our aim was to analyze mortality in a perinatal risk cohort of 46-year-old adults with childhood ADHD (cADHD) and milder childhood attention problems (including hyperactivity and inattention; cAP) compared with a group with similar birth risks but no or low levels of childhood ADHD symptoms (Non-cAP). Causes of death obtained from a national register were examined. Methods Mortality was analyzed with Cox proportional hazard models for all-cause mortality, cause-specific mortality (natural and unnatural causes), and age-specific mortality (under and over age 30). All models were adjusted with gender. The total n in the study was 839 (cADHD n = 115; cAP n = 216; Non-cAP n = 508). Results By the age of 46, 11 (9.6%) deaths occurred in the cADHD group, 7 (3.2%) in the cAP group, and 20 (3.9%) in the Non-cAP group. The cADHD group had the highest mortality risk (adjusted hazard ratio = 2.15; 95% CI 1.02, 4.54). Mortality was not elevated in the cAP group (adjusted hazard ratio = 0.72; 95% CI .30, 1.72). Mortality in the cADHD group was mainly attributed to unnatural causes of death (adjusted hazard ratio = 2.82; 95% CI 1.12, 7.12). The mortality risk in the cADHD group was sixfold before age 30 (adjusted hazard ratio = 6.20; 95% CI 1.78, 21.57). Conclusions Childhood ADHD was associated with a twofold risk of premature death by the age of 46 in this prospective longitudinal cohort study. Our results corroborate previous findings and the morbidity of ADHD. Subthreshold levels of childhood ADHD symptoms were not linked to increased mortality. Our results suggest that mortality risk is higher in young than middle adulthood. Future studies should examine mortality associated with ADHD in different ages in adulthood to identify those in greatest risk of premature death.