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Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both highly heritable neurodevelopmental disorders. Evidence indicates both disorders co-occur with a high frequency, in 20–50% of children with ADHD meeting criteria for ASD and in 30-80% of ASD children meeting criteria for ADHD. This review will provide an overview on all available studies [family based, twin, candidate gene, linkage, and genome wide association (GWA) studies] shedding light on the role of shared genetic underpinnings of ADHD and ASD. It is concluded that family and twin studies do provide support for the hypothesis that ADHD and ASD originate from partly similar familial/genetic factors. Only a few candidate gene studies, linkage studies and GWA studies have specifically addressed this co-occurrence, pinpointing to some promising pleiotropic genes, loci and single nucleotide polymorphisms (SNPs), but the research field is in urgent need for better designed and powered studies to tackle this complex issue. We propose that future studies examining shared familial etiological factors for ADHD and ASD use a family-based design in which the same phenotypic (ADHD and ASD), candidate endophenotypic, and environmental measurements are obtained from all family members. Multivariate multi-level models are probably best suited for the statistical analysis.

This study focused on the degree of report bias in assessing autistic traits. Both parents of 124 preschoolers completed the Social Communication Questionnaire and the Autism-spectrum Quotient. Acceptable agreement existed between mother and father reports of children’s mean scores of autistic traits, but interrater reliability for rank-order correlations was only fair. No evidence was found for report bias regarding parent-offspring autistic traits. However, adult autistic ratings were strongly biased: spouse-ratings were higher than self-ratings, correlations were only fair when both parents reported about the same person, and resemblance was higher for reports from the same person than for spouses’ separate self-reports. It is advisable to involve multiple informants when assessing autistic traits, and to use procedural and/or statistical remedies to control for report bias.

This study investigated the role of parental Autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and depressive symptoms on parenting stress in 174 families with children with ASD and/or ADHD, using generalized linear models and structural equation models. Fathers and mothers reported more stress when parenting with their child with ASD and/or ADHD than when parenting with the unaffected sibling; they also experienced more stress than a norm population. Depressive symptoms were most pronounced in the parents of children with ASD and ASD+ADHD. Spouse correlations were found for ASD, depression, and parenting stress. Paternal ASD and maternal ADHD symptoms were related to increased parenting stress, and parental ADHD symptoms with depressive symptoms and parenting stress. The results highlight the increased burden of raising a child with ASD and/or ADHD and the reciprocal relationship this has with parents’ ASD, ADHD, and depressive symptoms, and levels of stress.

Autism spectrum disorder (ASD) and Attention-deficit/hyperactivity disorder (ADHD) are often comorbid. The purpose of this study is to explore the relationships between ASD and ADHD symptoms by applying causal modeling. We used a large phenotypic data set of 417 children with ASD and/or ADHD, 562 affected and unaffected siblings, and 414 controls, to infer a structural equation model using a causal discovery algorithm. Three distinct pathways between ASD and ADHD were identified: (1) from impulsivity to difficulties with understanding social information, (2) from hyperactivity to stereotypic, repetitive behavior, (3) a pairwise pathway between inattention, difficulties with understanding social information, and verbal IQ. These findings may inform future studies on understanding the pathophysiological mechanisms behind the overlap between ASD and ADHD.

To advance understanding of the heterogeneity in the course of ADHD, joint symptom trajectories of inattention and hyperactivity-impulsivity from childhood to young adulthood were modelled and associated with genetic, demographic, and clinical characteristics. Data were obtained from the NeuroIMAGE cohort which includes 485 individuals with ADHD, their 665 siblings, and 399 typically developing children. Trajectories were based on scores of the Conners Parent Rating Scale Revised and estimated over seven homogeneous age bins (from 5 to 28 years) using parallel process latent class growth analysis on data collected across 2–4 time points. Multilevel multinomial logistic regression was used to identify characteristics that differentiated between the derived classes. A seven-class solution revealed “severe combined stable” (4.8%), “severe combined decreasing” (13%), “severe inattentive stable” (4.8%), “moderate combined increasing” (7.5%), “moderate combined decreasing” (12.7%), “stable mild” (12.9%), and “stable low” (44.3%) classes. Polygenic risk for depression, ADHD diagnosis, ADHD medication use, IQ, comorbid symptom levels (foremost oppositional behaviour), and functional impairment levels differentiated classes with similar ADHD symptom levels in childhood but a diverging course thereafter. The course of ADHD is highly heterogeneous, with stable, decreasing, and increasing trajectories. Overall, severe symptom levels in childhood are associated with elevated-to-severe symptom levels in adolescence and young adulthood, despite substantial symptom reductions. Beyond symptom severity in childhood, genetic, demographic, and clinical characteristics distinguish the heterogeneous course.

In this investigation, zinc oxide nanoparticles (ZnO NPs) were produced by solution combustion-assisted technique utilising aqueous leaf extract of Piper betle (betel leaf) (PB). Phase formation and the particle size of ZnO-PB-NPs were ascertained by using X-ray diffraction. It was observed that the ZnO-PB-NPs crystallize in the hexagonal phase with an average crystallite size of 24 nm. The morphology, shape, and size of the NPs were studied by Scanning Electron Microscope and Transmission Electron Microscope (TEM). The elemental composition was analysed using energy-dispersive advanced X-ray spectroscopy. Further, Fourier-Transform Infrared (FTIR) spectroscopy confirmed the formation of ZnO bonding. Anticancer activity of ZnO-PB-NPs was evaluated in the MDA-MB-231, human breast cancer cells by MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide] assay. The study findings demonstrated that the ZnO-PB-NPs were able to induce significant cytotoxicity in human breast cancer cells in a dose-dependent manner. ZnO-PB-NPs treatment impaired the Clonogenic potential cells of breast cancer. Additionally, the biocompatibility with blood components of ZnO-PB-NPs was evaluated by blood hemolysis assay. It was observed that, ZnO NPs inhibited breast cancer cell growth and increased the induction of early apoptosis cell population.

Cognitive research proposes that social cognition (SC), executive functions (EF) and local processing style (weak CC) may be fruitful areas for research into the familial-genetic underpinnings of Autism Spectrum Disorders (ASD). The performance of 140 children with ASD, 172 siblings and 127 controls on tasks measuring SC (face recognition, affective prosody, and facial emotion recognition), EF (inhibition, cognitive flexibility, and verbal working memory) and local processing style was assessed. Compelling evidence was found for the interrelatedness of SC and EF, but not local processing style, within individuals and within families, suggesting that these domains tend to co-segregate in ASD. Using the underlying shared variance of these constructs in genetic research may increase the power for detecting susceptibility genes for ASD.

Purpose Callous–unemotional (CU) traits are currently viewed as the defining signs and symptoms of juvenile psychopathy. It is unclear, however, whether CU traits have validity only in the context of conduct disorder (CD) as proposed by Frick and Moffitt (A proposal to the DSM-V childhood disorders and the ADHD and disruptive behavior disorders work groups to include a specifier to the diagnosis of conduct disorder based on the presence of callous–unemotional traits, American Psychiatric Association, Washington, DC, 2010 ), or also outside CD, either in combination with other forms of psychopathology or as a stand-alone construct. Methods The current review systematically studied the existent literature on CU traits in juveniles to examine their validity inside and outside CD according to the framework regarding the validity of a psychiatric diagnosis provided by Robins and Guze (Am J Psychiatry 126:983–987, 1970 ). Results Inside youth with conduct problems, and CD specifically, it seems that CU traits meet the Robins and Guze criteria. As many of the reviewed studies included youth with ODD and ADHD as well, there are indications the same might be true for ODD and ADHD, although probably to a lesser extent. In other disorders, CU traits may be present as well, but their role is not firmly established. As stand-alone construct, data are lacking or are scarce on all of the above-mentioned criteria. Conclusions CU traits are a useful specifier in CD, and possibly also in disruptive behaviour disorders (DBDs) more generally. High CU traits outside DBDs exist but it is as yet unknown if there is a clinical need for defining CU traits as a stand-alone construct.

There are very few studies on the long-term outcome of children and adolescents with ADHD-combined type in Europe. The objective of the present study is to assess the 6-year outcome (including pharmacological treatment) of a large cohort of participants with ADHD-combined type ( N  = 347, mean age 11.4 years) in late adolescence and early adulthood. At study entry and follow-up (mean age 17.4 years), participants were comprehensively assessed on ADHD and comorbid disorders by structured psychiatric interviews and multi-informant questionnaires. Overall functioning was assessed by the Children’s Global Assessment Scale. The retention rate was 75.6 %. The majority of participants (86.5 %) persisted in a DSM-5 ADHD diagnosis, 8.4 % had a subthreshold diagnosis, and 5.1 % remitted from the disorder at follow-up. Comorbidities decreased strongly; oppositional defiant disorder: 58 > 31 %, conduct disorder: 19 > 7 %. At follow-up, mood- and anxiety disorders were virtually non-existent following strict criteria (1–3 %). Percentage of children having had pharmacological treatment at any time increased from 79 to 91 %. On the Children’s Global Assessment Scale, 48.5 % of participants were still functionally impaired at follow-up. Parental ADHD, higher ADHD symptom severity at baseline and higher parent-reported impairment at baseline positively predicted current ADHD symptom severity ( R 2  = 20.9 %). Younger baseline age, higher ADHD symptom severity at baseline and higher parent-reported impairment at baseline were positively associated with poorer overall functioning ( R 2  = 17.8 %). Pharmacological treatment had no (beneficial) impact on either ADHD symptom severity or overall functioning. Results confirm that ADHD is largely persistent into late adolescence with severity and family history for the disorder as important risk factors.

Children with an autism spectrum disorder (ASD) and their unaffected siblings from 54 simplex (SPX, one individual in the family affected) and 59 multiplex (MPX, two or more individuals affected) families, and 124 controls were assessed on intelligence, social cognition and executive functions. SPX and MPX ASD probands displayed similar cognitive profiles, but within-family contrasts were highest in SPX families, suggesting SPX-MPX stratification may help parse etiological heterogeneity of ASD. Unaffected siblings (regardless SPX or MPX) were mostly unimpaired, suggesting that cognitive problems may be part of the defining features of ASD, rather than being an endophenotypic trait. Except for affective prosody, which appeared to be the most sensitive cognitive marker for detecting familial risk for ASD.