The COVID-19 outbreak and lockdown have been associated with multiple consequences for mental health, including an excessive and potentially harmful increase in screen media use. The specific consequences for children, adolescents and young adults with ADHD are still unknown. In the first part of this study, a short review of problematic use of the internet (PUI) in ADHD is presented, showing that patients with ADHD are at risk for different aspects of PUI, such as excessive gaming or problematic social media use. In the second part, we report original data of an online survey on screen media use before, during and after the lockdown completed by parents of children and adolescents clinically referred for ADHD. Parents rated children’s/adolescents’ media-related behavior and media time on a new screening questionnaire for PUI. Each item was rated three times, referring to the observed behavior before, during and 1–2 months after the lockdown. N = 126 parents of patients referred for ADHD aged 10–18 years participated in the study. Total media time increased by 46% during the lockdown and did not completely return to pre-Corona levels afterwards. Patients with difficulties concentrating, high irritability or deterioration of ADHD problems under lockdown spent more time with screen media than those with milder or no such problems. While the effects of the lockdown on screen media use and its negative impact on everyday life appear to be largely reversible, a small proportion of patients with ADHD apparently continue to show increased media use.
Attention-deficit hyperactivity disorder (ADHD) has been postulated to associate with dopaminergic dysfunction, including the dopamine transporter (DAT1). Several meta-analyses showed small but significant association between the 10-repeat allele in the DAT1 gene in 3′-untranslated region variant number tandem repeat polymorphism and child and adolescent ADHD, whereas in adult ADHD the 9-repeat allele was suggested to confer as risk allele. Interestingly, recent evidence indicated that the long-allele variants (10 repeats and longer) might confer to lower expression of the transporter in comparison to the short-allele. Therefore, we assessed here the association in samples consisting of families with child and adolescent ADHD as well as a case-control sample, using either the 10-versus 9-repeat or the long-versus short-allele approach. Following, we conducted a systematic review and meta-analysis, including family and case-control studies, using the two aforementioned approaches as well as stratifying to age and ethnicity. The first approach (10-repeat) resulted in nominal significant association in child and adolescent ADHD (OR 1.1050 p = 0.0128), that became significant stratifying to European population (OR 1.1301 p = 0.0085). The second approach (long-allele) resulted in significant association with the whole ADHD population (OR 1.1046 p = 0.0048), followed by significant association for child and adolescent ADHD (OR 1.1602 p = 0.0006) and in Caucasian and in European child and adolescent ADHD (OR 1.1310 p = 0.0114; OR 1.1661 p = 0.0061; respectively). We were not able to confirm the association reported in adults using both approaches. In conclusion, we found further indication for a possible DAT1 gene involvement; however, further studies should be conducted with stringent phenotyping to reduce heterogeneity, a limitation observed in most included studies.
Assuming that MCCs originate from Merkel cells, our data indicate a switch from E- and P-cadherin to N-cadherin during tumorigenesis. Whether the unexpected heterogeneity of junctional proteins can be exploited for prognostic and therapeutic purposes will need to be examined.
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