ADHD Atten Def Hyp Disord (2019) 11(Suppl 1):S1–S89 https://doi.org/10.1007/s12402-019-00295-7 ABSTRACTS Ó Springer-Verlag GmbH Austria, part of Springer Nature 2019 7th World Congress on ADHD: From Child to Adult Disorder 25th–28th April, Lisbon Portugal Editors: Manfred Gerlach, Wu¨rzburg Peter Riederer, Wu¨rzburg Andreas Warnke, Wu¨rzburg Luis Rohde, Porto Alegre 123 S2 ABSTRACTS Introduction Dear Colleagues and Friends, We are pleased to have received more than 180 poster abstracts as well as more than 100 poster abstracts from young scientists and clinicians (\ 35 years) who applied for our Young Scientists’ Award. Of all abstracts submitted by our young colleagues, the Scientific Programme Committee has selected the best eight. The authors have been invited to give a presentation as part of our two Young Scientist Award Sessions and to receive a prize money in the amount of 500 Euros. With this approach, we intend to highlight the importance of original scientific contributions, especially from our young colleagues. In this volume, the abstracts of our two Young Scientist Award Sessions come first, followed by regular poster abstracts. These have been organized by topics: Aetiology, Autism Spectrum Disorders, Co-morbidity, Diagnosis, Electrophysiology, Epidemiology, Experimental Models, Genetics, Neuroimaging, Non-pharmacological Treatment, Pathophysiology, Pharmacological Treatment, Quality of Life/Caregiver Burden, Substance Use Disorders and Miscellaneous. Submitted abstracts have not been modified in any way. Please, do not just read the selected poster abstracts, we also encourage you to actively discuss and share your ideas with our young colleagues. Finally, we would like thank all our speakers, contributors and sponsors of our 7th World Congress on ADHD: from Childhood to Adult Disease, and welcome you to join—what we are sure will be—a very enjoyable and highly informative event. Thank you very much for your participation! With kind regards, Luis Rohde Congress President President World Federation of ADHD Manfred Gerlach Chairmen Scientific Programme Committee 123 7th World Congress on ADHD: From Child to Adult Disorder S3 Young Scientists Awards Methods: To test this hypothesis, we obtained postmortem brain RNA-sequencing data from unaffected donors from the Allen Brain Atlas for cortical and subcortical regions that were analyzed by the Effects of methylphenidate on sleep in children ENIGMA-ADHD Working Group. We extracted expression levels of with ADHD gene sets that were selected based on hypotheses derived from prior work. We performed deconvolution of the bulk transcriptomic data I. Ferreira*, A. Amorim, C. Costa, B. Salgueiro, T. Aguiar, from the Allen Brain Atlas to determine the typical abundance of F. Fonseca, H. Loureiro neuronal and non-neuronal cells per brain region. We tested the correlation between gene set expression levels, cell abundance, and *Hospitalar Prof.Dr. Fernando Fonseca, Linda-a-Velha, Portugal regional changes in brain sizes observed in ADHD cases. Results: We found statistically significant correlations between Objectives: Sleep disorders are frequent amongst children and ado- reductions in brain region size in ADHD cases and expression levels lescents with ADHD and can add to the impairment of the disorder. of genes involved in apoptosis, autophagy, and neurodevelopment. Stimulant medication like methylphenidate (MPH) can also have an Furthermore, we identified significant associations between reduc- impact on sleep. The goal of our study was to analyse sleep archi- tions in regional brain size in ADHD and abundance of glial and tecture of children with ADHD and the impact of MPH on sleep. progenitor cell types. Methods: Retrospective analysis of the clinical records of children Conclusions: We conclude that expression levels of gene sets with ADHD that performed polysomnography (PSG type I) between involved in brain development and response to cell stress, coupled January 2016 and December 2018. We divided the sample into two with the organization of brain cell types, may contribute to selective groups: group A, with MPH and group B, without MPH, and com- brain region vulnerability in ADHD. pared sleep patterns. To analyse statistical significance, we used StataCorp. 2009. Stata Statistical Software and Wilcoxon Mann Whitney/T-student tests. Results: Total of 72 patients with ADHD. The most frequent ADHD Neurocognitive markers of late-onset ADHD: a 6-year subtype was inattentive (32%). Comparing sleep architecture between longitudinal study group A (n = 41/55%) and group B (n = 31/41%): mean Sleep effi- ciency was higher in group B (B 83.8%/A 78.1%) with statistical significance (p = 0.0498). Not statistically significant: Mean sleep S. Ilbegi*, J. K. Buitelaar, P. Hoekstra, C. Hartman, B. Franke, latency (A 33.5 min/B 31 min p = 0.8645). Mean duration of Stage S. Faraone, M. Luman, M. van Lieshout, N. Rommelse N2 (A 58.6 min/B 60.5 min. p = 0.2151), mean duration of Stage N3 (A 27.2 min/B 25.1 min. p = 0.1777), mean REM sleep latency (A *Radboud Univers. Medisch Centrum, Arnhem, The Netherlands 159.8 min/B 180.4 min. p = 0.1812) and mean REM sleep (A 13.2%/ Objectives: There is increased interest in ‘late-onset’ ADHD, refer- B 13.7%. p = 0.6516). Obstructive sleep apnoea (OSA) was frequent ring to the onset of clinically significant ADHD symptoms after the in both groups (group A 82%/B 87%), but differences weren’t sig- age 12, i.e. in adolescence or adulthood. Biological siblings of ADHD nificant (p = 0.4061). probands who are unaffected in childhood may be at increased risk for Conclusions: Our results suggest that MPH does not affect signifi- developing late-onset of ADHD. cantly sleep architecture, except for sleep efficiency. Our revision of Aim: To examine whether unaffected siblings with late-onset ADHD the literature also found few consistent findings. We highlight the fact could be differentiated from stable unaffected siblings by their neu- that OSA was a predominant feature and should be evaluated in these rocognitive functioning in childhood. patients, since it knowledgeably influences sleep architecture. We Methods: We report findings from a 6-year prospective, longitudinal acknowledge however that finding a relationship between sleep and study of a subsample of the Dutch part of the International Multi- medication is complex, because other sample characteristics may center ADHD Genetics (IMAGE) study, including individuals with impact sleep findings, and thus influence results. childhood-onset (persistent) ADHD (n = 111), late-onset ADHD (n = 34), stable unaffected siblings (n = 111), and healthy controls (n = 186). At study entry (mean age: 11.3) and follow-up (mean age: 17.01) participants were comprehensively assessed on ADHD by Genes and brain cell types linked with selective structured psychiatric interviews and multi-informant questionnaires. neuronal vulnerability in ADHD Several neurocognitive functions including time reproduction, timing variability (reaction time variability and time production variability), J. Hess*, J. Patak, S. Glatt, S. Faraone reaction time speed, motor control, working memory, and intelligence were assessed at baseline and after 6 years. *SUNY Upstate, Syracuse, USA Results: Siblings with late-onset ADHD were similar to individuals with childhood-onset ADHD in showing longer reaction times and/or Objectives: A series of large multi-site mega-analyses of structural higher error rates on all neurocognitive measures at baseline and brain imaging data led by the Enhancing Neuroimaging Genetics follow-up, when compared to healthy controls; they differed from through Meta-analysis (ENGIMA) Network found specific cortical stable unaffected siblings by greater reaction time variability and and subcortical regions that are significantly smaller in individuals timing production variability at baseline. No significant group by time diagnosed with attention-deficit/hyperactivity disorder (ADHD) interaction was present for all tasks. compare to unaffected controls. Those studies provided important Conclusions: Neurocognitive dysfunction, in particular for reaction insight into neuroanatomical changes in ADHD, but it is unclear why time variability and timing production variability, may serve among some brain regions are affected by ADHD while other regions remain unaffected siblings as risk biomarkers for late-onset ADHD. spared. We hypothesized that spatial variation in the organization of brain cells and/or gene expression levels across brain regions may contribute to selective neuroanatomical changes seen in ADHD. 123 S4 ABSTRACTS Genetic alteration of CADM1 is associated with ADHD Early predictors for late-onset ADHD symptoms during early life: an exploratory study with genetic, neuroimaging and animal model methods C. K. Liu*, J.-B. Pingault, P. Asherson, C. Greven, E. Viding *University College of London, London, UK J. Jin*, L. Liu, Q. Gao, H. Li, Y. Wang, Q. Qian Objectives: ADHD has been conceptualised as a childhood-onset *University of Beijing, Peking, People’s Republic of China neurodevelopmental disorder. However, a considerable number of studies have identified the emergence of ADHD symptoms beyond Objectives: Genes related to cell adhesion pathway is thought to the childhood years. In addition, different childhood characteristics contribute to the genetic architecture of Attention-Deficit Hyperac- were found between late-onset of ADHD and early-onset ADHD. tivity Disorder (ADHD). Cell adhesion molecule 1 (CADM1) is cell Despite the increasing knowledge