@article {367, title = {Developmental co-occurrence of psychopathology dimensions in childhood}, journal = {JCPP Advances}, volume = {2}, year = {2022}, pages = {e12100}, abstract = {

Background: Comorbidity between psychopathologies may be attributed to genetic and environmental differences between people as well as causal processes within individuals, where one pathology increases risk for another. Disentangling between-person (co)variance from within-person processes of psychopathology dimensions across childhood may shed light on developmental causes of comorbid mental health problems. Here, we aim to determine whether and to what extent directional relationships between psychopathology dimensions within-person, and between individuals within families, play a role in comorbidity. Methods: We conducted random intercepts cross-lagged panel model (RI-CLPM) analyses to unravel the longitudinal co-occurrence of child psychopathology dimensions, jointly estimating between-person and within-person processes from childhood to early adolescence (age 7-12). We further developed an extension of the model to estimate sibling effects within-family (wf-RI-CLPM). Analyses were separately conducted in two large population-based cohorts, TEDS and NTR, including parent-rated measures of child problem behaviours based on the SDQ and CBCL scales respectively. Results: We found evidence for strong between-person effects underlying the positive intercorrelation between problem behaviours across time. Beyond these time-varying within-person processes accounted for an increasing amount of trait variance, within- and cross-trait, overtime in both cohorts. Lastly, by accommodating family level data, we found evidence for reciprocal directional influences within sib-pairs longitudinally. Conclusions: Our results indicate that within-person processes partly explain the co-occurrence of psychopathology dimensions across childhood, and within sib-pairs. Analyses provided substantive results on developmental processes underlying comorbidity in behavioural problems. Future studies should consider different developmental timeframes to shed more light on the processes contributing to developmental comorbidity.

}, keywords = {comorbidity, development, genetic and environmental effects, psychopathology, sibling effects}, doi = {10.1002/jcv2.12100}, author = {Allegrini, Andrea G and van Beijsterveldt, Toos and Boomsma, Dorret I and Rimfeld, Kaili and Pingault, Jean-Baptiste and Plomin, Robert and Bartels, Meike and Nivard, Michel G} } @article {368, title = {Discovery of 42 genome-wide significant loci associated with dyslexia}, journal = {Nature Genetics}, volume = {54}, year = {2022}, pages = {1621{\textendash}1629}, abstract = {

Reading and writing are crucial life skills but roughly one in ten children are affected by dyslexia, which can persist into adulthood. Family studies of dyslexia suggest heritability up to 70\%, yet few convincing genetic markers have been found. Here we performed a genome-wide association study of 51,800 adults self-reporting a dyslexia diagnosis and 1,087,070 controls and identified 42 independent genome-wide significant loci: 15 in genes linked to cognitive ability/educational attainment, and 27 new and potentially more specific to dyslexia. We validated 23 loci (13 new) in independent cohorts of Chinese and European ancestry. Genetic etiology of dyslexia was similar between sexes, and genetic covariance with many traits was found, including ambidexterity, but not neuroanatomical measures of language-related circuitry. Dyslexia polygenic scores explained up to 6\% of variance in reading traits, and might in future contribute to earlier identification and remediation of dyslexia.

}, doi = {10.1038/s41588-022-01192-y}, author = {Doust, Catherine and Fontanillas, Pierre and Eising, Else and Gordon, Scott D and Wang, Zhengjun and Alag{\"o}z, G{\"o}kberk and Molz, Barbara and 23andMe Research Team and Quantitative Trait Working Group of the GenLang Consortium and Pourcain, Beate St and Francks, Clyde and Marioni, Riccardo E and Zhao, Jingjing and Paracchini, Silvia and Talcott, Joel B and Monaco, Anthony P and Stein, John F and Gruen, Jeffrey R and Olson, Richard K and Willcutt, Erik G and DeFries, John C and Pennington, Bruce F and Smith, Shelley D and Wright, Margaret J and Martin, Nicholas G and Auton, Adam and Bates, Timothy C and Fisher, Simon E and Luciano, Michelle} } @article {376, title = {DNA methylation in peripheral tissues and left-handedness}, journal = {Nature Scientific Reports}, volume = {12}, year = {2022}, pages = {5606}, abstract = {

Handedness has low heritability and epigenetic mechanisms have been proposed as an etiological mechanism. To examine this hypothesis, we performed an epigenome-wide association study of left-handedness. In a meta-analysis of 3914 adults of whole-blood DNA methylation, we observed that CpG sites located in proximity of handedness-associated genetic variants were more strongly associated with left-handedness than other CpG sites (P = 0.04), but did not identify any differentially methylated positions. In longitudinal analyses of DNA methylation in peripheral blood and buccal cells from children (N = 1737), we observed moderately stable associations across age (correlation range [0.355-0.578]), but inconsistent across tissues (correlation range [- 0.384 to 0.318]). We conclude that DNA methylation in peripheral tissues captures little of the variance in handedness. Future investigations should consider other more targeted sources of tissue, such as the brain.

}, doi = {10.1038/s41598-022-08998-0}, author = {Odintsova, Veronika V and Suderman, Matthew and Hagenbeek, Fiona A and Caramaschi, Doretta and Hottenga, Jouke-Jan and Pool, Ren{\'e} and BIOS Consortium and Dolan, Conor V and Ligthart, Lannie and van Beijsterveldt, Catharina E M and Willemsen, Gonneke and de Geus, Eco J C and Beck, Jeffrey J and Ehli, Erik A and Cuellar-Partida, Gabriel and Evans, David M and Medland, Sarah E and Relton, Caroline L and Boomsma, Dorret I and van Dongen, Jenny} } @inbook {351, title = {Discordant monozygotic twin studies of epigenetic mechanisms in mental health}, booktitle = {Twin and Family Studies of Epigenetics}, volume = {27}, number = {Translational Epigenetics}, year = {2021}, pages = {43{\textendash}66}, publisher = {Elsevier}, organization = {Elsevier}, chapter = {3}, abstract = {

The discordant monozygotic twin design is a strong method to assess causality. The design has been applied in a number of studies to investigate epigenetic mechanisms associated with mental health. These studies initially mainly focused on candidate genes and increasingly on genome-wide DNA methylation, gene expression, and X-chromosome inactivation, in various surrogate tissues such as blood and buccal cells, but also in brain tissue. In this chapter we review monozygotic twin studies of autism, aggressive behavior, ADHD, schizophrenia, bipolar disorder, and depression. We discuss the insights obtained by these studies and describe current limitations and challenges, including sample size, the use of surrogate tissues, causality, and confounders that apply to studies of cognitive and mental health such as medication use, lifestyle, and cellular heterogeneity of commonly investigated tissues.

}, doi = {https://doi.org/10.1016/B978-0-12-820951-6.00003-X}, author = {van Dongen, Jenny and Odintsova, Veronika V and Boomsma, Dorret I} } @article {349, title = {DNA methylation signatures of aggression and closely related constructs: A meta-analysis of epigenome-wide studies across the lifespan}, journal = {Molecular Psychiatry}, volume = {26}, year = {2021}, pages = {2148{\textendash}2162}, abstract = {

DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 $\times$ 10-7; Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83\% of these sites showed the same direction of association with childhood aggression (r = 0.7

}, doi = {10.1038/s41380-020-00987-x}, author = {van Dongen, Jenny and Hagenbeek, Fiona A and Suderman, Matthew and Roetman, Peter J and Sugden, Karen and Chiocchetti, Andreas G and Ismail, Khadeeja and Mulder, Rosa H and Hafferty, Jonathan D and Adams, Mark J and Walker, Rosie M and Morris, Stewart W and Lahti, Jari and K{\"u}pers, Leanne K and Escaramis, Georgia and Alemany, Silvia and Jan Bonder, Marc and Meijer, Mandy and Ip, Hill F and Jansen, Rick and Baselmans, Bart M L and Parmar, Priyanka and Lowry, Estelle and Streit, Fabian and Sirignano, Lea and Send, Tabea S and Frank, Josef and Jylh{\"a}v{\"a}, Juulia and Wang, Yunzhang and Mishra, Pashupati Prasad and Colins, Olivier F and Corcoran, David L and Poulton, Richie and Mill, Jonathan and Hannon, Eilis and Arseneault, Louise and Korhonen, Tellervo and Vuoksimaa, Eero and Felix, Janine F and Bakermans-Kranenburg, Marian J and Campbell, Archie and Czamara, Darina and Binder, Elisabeth and Corpeleijn, Eva and Gonzalez, Juan R and Grazuleviciene, Regina and Gutzkow, Kristine B and Evandt, Jorunn and Vafeiadi, Marina and Klein, Marieke and van der Meer, Dennis and Ligthart, Lannie and BIOS Consortium and Kluft, Cornelis and Davies, Gareth E and Hakulinen, Christian and Keltikangas-J{\"a}rvinen, Liisa and Franke, Barbara and Freitag, Christine M and Konrad, Kerstin and Hervas, Amaia and Fern{\'a}ndez-Rivas, Aranzazu and Vetro, Agnes and Raitakari, Olli and Lehtim{\"a}ki, Terho and Vermeiren, Robert and Strandberg, Timo and R{\"a}ikk{\"o}nen, Katri and Snieder, Harold and Witt, Stephanie H and Deuschle, Michael and Pedersen, Nancy L and H{\"a}gg, Sara and Sunyer, Jordi and Franke, Lude and Kaprio, Jaakko and Ollikainen, Miina and Moffitt, Terrie E and Tiemeier, Henning and van IJzendoorn, Marinus H and Relton, Caroline and Vrijheid, Martine and Sebert, Sylvain and Jarvelin, Marjo-Riitta and Caspi, Avshalom and Evans, Kathryn L and McIntosh, Andrew M and Bartels, Meike and Boomsma, Dorret I} } @article {324, title = {Data integration methods for phenotype harmonization in multi-cohort genome-wide association studies with behavioral outcomes}, journal = {Frontiers in Genetics}, volume = {10}, year = {2019}, pages = {1227}, abstract = {

Parallel meta-analysis is a popular approach for increasing the power to detect genetic effects in genome-wide association studies across multiple cohorts. Consortia studying the genetics of behavioral phenotypes are oftentimes faced with systematic differences in phenotype measurement across cohorts, introducing heterogeneity into the meta-analysis and reducing statistical power. This study investigated integrative data analysis (IDA) as an approach for jointly modeling the phenotype across multiple datasets. We put forth a bi-factor integration model (BFIM) that provides a single common phenotype score and accounts for sources of study-specific variability in the phenotype. In order to capitalize on this modeling strategy, a phenotype reference panel was utilized as a supplemental sample with complete data on all behavioral measures. A simulation study showed that a mega-analysis of genetic variant effects in a BFIM were more powerful than meta-analysis of genetic effects on a cohort-specific sum score of items. Saving the factor scores from the BFIM and using those as the outcome in meta-analysis was also more powerful than the sum score in most simulation conditions, but a small degree of bias was introduced by this approach. The reference panel was necessary to realize these power gains. An empirical demonstration used the BFIM to harmonize aggression scores in 9-year old children across the Netherlands Twin Register and the Child and Adolescent Twin Study in Sweden, providing a template for application of the BFIM to a range of different phenotypes. A supplemental data collection in the Netherlands Twin Register served as a reference panel for phenotype modeling across both cohorts. Our results indicate that model-based harmonization for the study of complex traits is a useful step within genetic consortia.

}, keywords = {consortia, data integration, genome-wide association studies, latent variable modeling, phenotype harmonization}, doi = {10.3389/fgene.2019.01227}, author = {Luningham, Justin M and McArtor, Daniel B and Hendriks, Anne M and van Beijsterveldt, Catharina E M and Lichtenstein, Paul and Lundstr{\"o}m, Sebastian and Larsson, Henrik and Bartels, Meike and Boomsma, Dorret I and Lubke, Gitta H} } @article {327, title = {DNA methylation signatures of breastfeeding in buccal cells collected in mid-childhood}, journal = {Nutrients}, volume = {11}, year = {2019}, pages = {2804}, abstract = {

Breastfeeding has long-term benefits for children that may be mediated via the epigenome. This pathway has been hypothesized, but the number of empirical studies in humans is small and mostly done by using peripheral blood as the DNA source. We performed an epigenome-wide association study (EWAS) in buccal cells collected around age nine (mean = 9.5) from 1006 twins recruited by the Netherlands Twin Register (NTR). An age-stratified analysis examined if effects attenuate with age (median split at 10 years; n10 = 489, mean age = 11.2). We performed replication analyses in two independent cohorts from the NTR (buccal cells) and the Avon Longitudinal Study of Parents and Children (ALSPAC) (peripheral blood), and we tested loci previously associated with breastfeeding in epigenetic studies. Genome-wide DNA methylation was assessed with the Illumina Infinium MethylationEPIC BeadChip (Illumina, San Diego, CA, USA) in the NTR and with the HumanMethylation450 Bead Chip in the ALSPAC. The duration of breastfeeding was dichotomized (\&$\#$39;never\&$\#$39; vs. \&$\#$39;ever\&$\#$39;). In the total sample, no robustly associated epigenome-wide significant CpGs were identified ($\alpha$ = 6.34 $\times$ 10-8). In the sub-group of children younger than 10 years, four significant CpGs were associated with breastfeeding after adjusting for child and maternal characteristics. In children older than 10 years, methylation differences at these CpGs were smaller and non-significant. The findings did not replicate in the NTR sample (n = 98; mean age = 7.5 years), and no nearby sites were associated with breastfeeding in the ALSPAC study (n = 938; mean age = 7.4). Of the CpG sites previously reported in the literature, three were associated with breastfeeding in children younger than 10 years, thus showing that these CpGs are associated with breastfeeding in buccal and blood cells. Our study is the first to show that breastfeeding is associated with epigenetic variation in buccal cells in children. Further studies are needed to investigate if methylation differences at these loci are caused by breastfeeding or by other unmeasured confounders, as well as what mechanism drives changes in associations with age.

}, keywords = {ALSPAC., breastfeeding, DNA methylation, EPIC, EWAS, NTR, twins}, doi = {10.3390/nu11112804}, author = {Odintsova, Veronika V and Hagenbeek, Fiona A and Suderman, Matthew and Caramaschi, Doretta and van Beijsterveldt, Catharina E M and Kallsen, Noah A and Ehli, Erik A and Davies, Gareth E and Sukhikh, Gennady T and Fanos, Vassilios and Relton, Caroline and Bartels, Meike and Boomsma, Dorret I and van Dongen, Jenny} } @article {280, title = {Developing SENSES: Student experience of non-shared environment scales}, journal = {PLOS ONE}, volume = {13}, year = {2018}, month = {09}, pages = {1-16}, abstract = {

Twin and adoption studies find that non-shared environmental (NSE) factors account for variance in most behavioural traits and offer an explanation for why genetically identical individuals differ. Using data from a qualitative hypothesis-generating study we designed a quantitative measure of pupils\’ non-shared experiences at the end of formal compulsory education (SENSES: Student Experiences of Non-Shared Environment Scales). In Study 1 SENSES was administered to n = 117 16\–19 year old twin pairs. Exploratory Factor Analysis yielded a 49-item 10 factor solution which explained 63\% of the variance in responses. SENSES showed good internal consistency and convergent and divergent validity. In Study 2 this factor structure was confirmed with data from n = 926 twin pairs and external validity was demonstrated via significant correlations between 9 SENSES factors and both public examination performance and life satisfaction. These studies lend preliminary support to SENSES but further research is required to confirm its psychometric properties; to assess whether individual differences in SENSES are explained by NSE effects; and to explore whether SENSES explains variance in achievement and wellbeing.

}, doi = {10.1371/journal.pone.0202543}, url = {https://doi.org/10.1371/journal.pone.0202543}, author = {Yerdelen, Sundus and Durksen, Tracy and Kaili Rimfeld and Robert Plomin and Asbury, Kathryn} } @article {259, title = {Differences in exam performance between pupils attending selective and non-selective schools mirror the genetic differences between them}, volume = {3}, year = {2018}, month = {2018/03/23}, pages = {3}, abstract = {

On average, students attending selective schools outperform their non-selective counterparts in national exams. These differences are often attributed to value added by the school, as well as factors schools use to select pupils, including ability, achievement and, in cases where schools charge tuition fees or are located in affluent areas, socioeconomic status. However, the possible role of DNA differences between students of different schools types has not yet been considered. We used a UK-representative sample of 4814 genotyped students to investigate exam performance at age 16 and genetic differences between students in three school types: state-funded, non-selective schools (\‘non-selective\’), state-funded, selective schools (\‘grammar\’) and private schools, which are selective (\‘private\’). We created a genome-wide polygenic score (GPS) derived from a genome-wide association study of years of education (EduYears). We found substantial mean genetic differences between students of different school types: students in non-selective schools had lower EduYears GPS compared to those in grammar (d\ =\ 0.41) and private schools (d\ =\ 0.37). Three times as many students in the top EduYears GPS decile went to a selective school compared to the bottom decile. These results were mirrored in the exam differences between school types. However, once we controlled for factors involved in pupil selection, there were no significant genetic differences between school types, and the variance in exam scores at age 16 explained by school type dropped from 7\% to \<1\%. These results show that genetic and exam differences between school types are primarily due to the heritable characteristics involved in pupil admission.

}, isbn = {2056-7936}, url = {https://doi.org/10.1038/s41539-018-0019-8}, author = {Emily Smith-Woolley and Pingault, Jean-Baptiste and Saskia Selzam and Kaili Rimfeld and Eva Krapohl and Sophie von Stumm and Asbury, Kathryn and Philip S. Dale and Young, Toby and Allen, Rebecca and Yulia Kovas and Robert Plomin} } @article {261, title = {DNA methylation age is associated with an altered hemostatic profile in a multi-ethnic meta-analysis}, journal = {Blood}, year = {2018}, abstract = {

Elevated epigenetic age is associated with an altered hemostatic factor profile and lower clotting time (aPTT).DNA methylation age is associated with mRNA levels of fibrinogen in multiple tissues. Many hemostatic factors are associated with age and age-related diseases, however much remains unknown about the biological mechanisms linking aging and hemostatic factors. DNA methylation is a novel means by which to assess epigenetic aging, which is a measure of age and the aging processes as determined by altered epigenetic states. We used a meta-analysis approach to examine the association between measures of epigenetic aging and hemostatic factors, as well as a clotting time measure. For fibrinogen, we used European and African-ancestry participants who were meta-analyzed separately and combined via a random effects meta-analysis. All other measures only included participants of European-ancestry. We found that 1-year higher extrinsic epigenetic age as compared to chronological age was associated with higher fibrinogen (0.004 g/L per year; 95\% CI: 0.001, 0.007; P = 0.01) and plasminogen activator inhibitor 1 (PAI-1; 0.13 U/mL per year; 95\% CI: 0.07, 0.20; P = 6.6x10-5) concentrations as well as lower activated partial thromboplastin time, a measure of clotting time. We replicated PAI-1 associations using an independent cohort. To further elucidate potential functional mechanisms we associated epigenetic aging with expression levels of the PAI-1 protein encoding gene (SERPINE1) and the three fibrinogen subunit-encoding genes (FGA, FGG, and FGB), in both peripheral blood and aorta intima-media samples. We observed associations between accelerated epigenetic aging and transcription of FGG in both tissues. Collectively, our results indicate that accelerated epigenetic aging is associated with a pro-coagulation hemostatic profile, and that epigenetic aging may regulate hemostasis in part via gene transcription.

}, issn = {0006-4971}, doi = {10.1182/blood-2018-02-831347}, url = {http://www.bloodjournal.org/content/early/2018/07/24/blood-2018-02-831347}, author = {Ward-Caviness, Cavin K. and Huffman, Jennifer E. and Evertt, Karl and Germain, Marine and van Dongen, Jenny and Hill, W. David and Jhun, Min A. and Brody, Jennifer A. and Ghanbari, Mohsen and Du, Lei and Roetker, Nicholas S. and de Vries, Paul S. and Waldenberger, Melanie and Gieger, Christian and Wolf, Petra and Prokisch, Holger and Koenig, Wolfgang and O{\textquoteright}Donnell, Christopher J. and Levy, Daniel and Liu, Chunyu and Truong, Vinh and Wells, Philip S. and Tr{\'e}gou{\"e}t, David-Alexandre and Tang, Weihong and Morrison, Alanna C. and Boerwinkle, Eric and Wiggins, Kerri L. and McKnight, Barbara and Guo, Xiuqing and Psaty, Bruce M. and Sotoodenia, Nona and Dorret I. Boomsma and Gonneke Willemsen and Lannie Ligthart and Deary, Ian J. and Zhao, Wei and Ware, Erin B. and Kardia, Sharon L.R. and Joyce B.J. Van Meurs and Uitterlinden, Andre G. and Franco, Oscar H. and Eriksson, Per and Franco-Cereceda, Anders and Pankow, James S. and Johnson, Andrew D. and Gagnon, France and Morange, Pierre-Emmanuel and de Geus, Eco J.C. and Starr, John M. and Smith, Jennifer A. and Dehghan, Abbas and Bj{\"o}rck, Hanna M. and Smith, Nicholas L. and Peters, Annette} } @article {227, title = {DNA methylation signatures of educational attainment}, volume = {3}, year = {2018}, month = {2018/03/23}, pages = {7}, abstract = {

Educational attainment is a key behavioural measure in studies of cognitive and physical health, and socioeconomic status. We measured DNA methylation at 410,746 CpGs (N\ =\ 4152) and identified 58 CpGs associated with educational attainment at loci characterized by pleiotropic functions shared with neuronal, immune and developmental processes. Associations overlapped with those for smoking behaviour, but remained after accounting for smoking at many CpGs: Effect sizes were on average 28\% smaller and genome-wide significant at 11 CpGs after adjusting for smoking and were 62\% smaller in never smokers. We examined sources and biological implications of education-related methylation differences, demonstrating correlations with maternal prenatal folate, smoking and air pollution signatures, and associations with gene expression in cis, dynamic methylation in foetal brain, and correlations between blood and brain. Our findings show that the methylome of lower-educated people resembles that of smokers beyond effects of their own smoking behaviour and shows traces of various other exposures.

}, isbn = {2056-7936}, url = {https://doi.org/10.1038/s41539-018-0020-2}, author = {Jenny van Dongen and Bonder, Marc Jan and Dekkers, Koen F. and Michel G. Nivard and van Iterson, Maarten and Gonneke Willemsen and Beekman, Marian and van der Spek, Ashley and Joyce B.J. Van Meurs and Franke, Lude and Bastiaan T. Heijmans and van Duijn, Cornelia M. and Slagboom, P. Eline and Dorret I. Boomsma} } @article {315, title = {Do parental psychiatric symptoms predict outcome in children with psychiatric disorders? A naturalistic clinical study}, journal = {Journal of the American Academy of Child \& Adolescent Psychiatry}, volume = {57}, year = {2018}, pages = {669{\textendash}677.e6}, abstract = {

OBJECTIVE: Parental psychiatric symptoms can negatively affect the outcome of children\&$\#$39;s psychopathology. Studies thus far have mainly shown a negative effect of maternal depression. This study examined the associations between a broad range of psychiatric symptoms in mothers and fathers and the child\&$\#$39;s outcome. METHOD: Internalizing and externalizing psychiatric symptoms were assessed in 742 mothers, 440 fathers, and their 811 children at the first evaluation in 3 child and adolescent psychiatric outpatient clinics and at follow-up (on average 1.7 years later). Predictions of child\&$\#$39;s symptoms scores were tested at follow-up by parental symptom scores at baseline, parental scores at follow-up, and offspring scores at baseline. RESULTS: Children whose mother or father scored above the (sub)clinical threshold for psychiatric symptoms at baseline had higher symptom scores at baseline and at follow-up. Offspring follow-up scores were most strongly predicted by offspring baseline scores, in addition to parental psychiatric symptoms at follow-up. Offspring symptom scores at follow-up generally were not predicted by parental scores at baseline. Maternal and paternal associations were of similar magnitude. CONCLUSION: Higher symptom scores at follow-up in children of parents with psychopathology were mainly explained by higher symptom scores at baseline. Continuing parent-offspring associations could be a result of reciprocal effects, ie, parental symptoms influencing offspring symptoms and offspring symptoms influencing parental symptoms. Nevertheless, the results show that these children are at risk for persisting symptoms, possibly indicating the need to treat maternal and paternal psychopathology.

}, keywords = {child psychopathology, longitudinal, parent-offspring associations, parental psychopathology}, doi = {10.1016/j.jaac.2018.05.017}, author = {Wesseldijk, Laura W and Dieleman, Gwen C and van Steensel, Francisca J A and Bleijenberg, Ellen J and Bartels, Meike and B{\"o}gels, Susan M and Middeldorp, Christel M} } @article {277, title = {During day and night: Childhood psychotic experiences and objective and subjective sleep problems}, journal = {Schizophrenia Research}, year = {2018}, abstract = {

Background
Psychotic experiences comprise auditory and visual perceptive phenomena, such as hearing or seeing things that are not there, in the absence of a psychotic disorder. Psychotic experiences commonly occur in the general pediatric population. Although the majority of psychotic experiences are transient, they are predictive of future psychotic and non-psychotic disorders. They have been associated with sleep problems, but studies with objective sleep measures are lacking. This study assessed whether psychotic experiences were associated with actigraphic sleep measures, symptoms of dyssomnia, nightmares, or other parasomnias.


Methods
This cross-sectional population-based study comprises 4149 children from the Generation R Study. At age 10 years, psychotic experiences including hallucinatory phenomena were assessed by self-report; dyssomnia and parasomnia symptoms were assessed by mother- and child-report. Additionally, at age 11 years, objective sleep parameters were measured using a tri-axial wrist accelerometer in N = 814 children, who wore the accelerometer for five consecutive school days.

Results
Psychotic experiences were not associated with objective sleep duration, sleep efficiency, arousal, or social jetlag. However, psychotic experiences were associated with self-reported dyssomnia (B = 2.45, 95\%CI: 2.13\–2.77, p \< 0.001) and mother-reported parasomnia, specifically nightmares (ORadjusted = 3.59, 95\%CI 2.66\–4.83, p \< 0.001). Similar results were found when analyses were restricted to hallucinatory phenomena.

Conclusions
Childhood psychotic experiences were not associated with objective sleep measures. In contrast, psychotic experiences were associated with nightmares, which are a known risk indicator of psychopathology in pre-adolescence. More research is needed to shed light on the potential etiologic or diagnostic role of nightmares in the development of psychotic phenomena.

}, keywords = {Actigraphy, General population, Hallucinatory phenomena, Parasomnia, Psychosis, Social jetlag}, issn = {0920-9964}, doi = {https://doi.org/10.1016/j.schres.2018.12.002}, url = {http://www.sciencedirect.com/science/article/pii/S0920996418306911}, author = {M. Elisabeth Koopman-Verhoeff and Koen Bolhuis and Charlotte A.M. Cecil and Desana Kocevska and J.J. Hudziak and Manon H.J. Hillegers and Viara R. Mileva-Seitz and Irwin K. Reiss and Liesbeth Duijts and Frank Verhulst and Maartje P.C.M. Luijk and Henning Tiemeier} } @article {192, title = {Disentangling Heterogeneity of Childhood Disruptive Behavior Problems Into Dimensions and Subgroups}, journal = {American Academy of Child and Adolescent Psychiatry. Journal}, volume = {56}, year = {2017}, pages = {678{\textendash}686}, abstract = {

OBJECTIVE:

Irritable and oppositional behaviors are increasingly considered as distinct dimensions of oppositional defiant disorder. However, few studies have explored this multidimensionality across the broader spectrum of disruptive behavior problems (DBPs). This study examined the presence of dimensions and distinct subgroups of childhood DBPs, and the cross-sectional and longitudinal associations between these dimensions.

METHOD:

Using factor mixture models (FMMs), the presence of dimensions and subgroups of DBPs was assessed in the Generation R Study at ages 6 (n\ = 6,209) and 10 (n\ =\ 4,724) years. Replications were performed in two population-based cohorts (Netherlands Twin Registry, n\ = 4,402, and Swedish Twin Study of Child and Adolescent Development, n\ = 1,089) and a clinical sample (n\ = 1,933). We used cross-lagged modeling in the Generation R Study to assess cross-sectional and longitudinal associations between dimensions. DBPs were assessed using mother-reported responses to the Child Behavior Checklist.

RESULTS:

Empirically obtained dimensions of DBPs were oppositional behavior (age 6 years), disobedient behavior, rule-breaking behavior (age 10 years), physical aggression, and irritability (both ages). FMMs suggested that one-class solutions had the best model fit for all dimensions in all three population-based cohorts. Similar results were obtained in the clinical sample. All three dimensions, including irritability, predicted subsequent physical aggression (range, 0.08-0.16).

CONCLUSION:

This study showed that childhood DBPs should be regarded as a multidimensional phenotype rather than comprising distinct subgroups. Incorporating multidimensionality will improve diagnostic accuracy and refine treatment. Future studies need to address the biological validity of the DBP dimensions observed in this study; herein lies an important opportunity for neuroimaging and genetic measures.

}, doi = {10.1016/j.jaac.2017.05.019}, author = {Koen Bolhuis and Gitta Lubke and van der Ende, Jan and Meike Bartels and van Beijsterveldt, Toos and Paul Lichtenstein and Henrik Larsson and Vincent W.V. Jaddoe and Steven A. Kushner and Frank Verhulst and Dorret I. Boomsma and Henning Tiemeier} } @article {129, title = {Discovery of biochemical biomarkers for aggression: A role for metabolomics in psychiatry.}, journal = {Am J Med Genet B Neuropsychiatr Genet}, year = {2016}, month = {2016 Feb 23}, abstract = {

Human aggression encompasses a wide range of behaviors and is related to many psychiatric disorders. We introduce the different classification systems of aggression and related disorders as a basis for discussing biochemical biomarkers and then present an overview of studies in humans (published between 1990 and 2015) that reported statistically significant associations of biochemical biomarkers with aggression, DSM-IV disorders involving aggression, and their subtypes. The markers are of different types, including inflammation markers, neurotransmitters, lipoproteins, and hormones from various classes. Most studies focused on only a limited portfolio of biomarkers, frequently a specific class only. When integrating the data, it is clear that compounds from several biological pathways have been found to be associated with aggressive behavior, indicating complexity and the need for a broad approach. In the second part of the paper, using examples from the aggression literature and psychiatric metabolomics studies, we argue that a better understanding of aggression would benefit from a more holistic approach such as provided by metabolomics. \© 2016 Wiley Periodicals, Inc.

}, issn = {1552-485X}, doi = {10.1002/ajmg.b.32435}, author = {Fiona Hagenbeek and Kluft, Cornelis and Thomas Hankemeier and Meike Bartels and Draisma, Harmen H M and Christel Middeldorp and Berger, Ruud and Antonio Noto and Lussu, Milena and Pool, Ren{\'e} and Faa, Gavino and Dorret I. Boomsma} } @article {75, title = {DisseminACTION: disseminating science in the information age (www.action-euproject.eu: a website for researchers and parents)}, journal = {Journal of Pediatric and Neonatal Individualized Medicine (JPNIM)}, volume = {4}, year = {2015}, month = {10/2015}, pages = {103-110}, type = {Proceedings of the 11{\textdegree} International Workshop on Neonatology and Satellite Meetings, Cagliari (Italy), October 26-31}, abstract = {

www.action-euproject.eu is a website designed at the University of Cagliari, by the Department of Surgery, Faculty of Medicine, within the project \“ACTION - Aggression in Children: unravelling gene-environment interplay to inform Treatment and InterventiON strategies\”, a collaborative project which includes twelve international partners, funded under the 7th Framework Programme for Research, technological Development and Demonstration.

Its aim is to properly disseminate official news, events, medical discoveries carried out within the project, with an intent to connect European researchers and citizens with the official source of ACTION\’s scientific research.

One of the main problems of the so called Web 2.0., is represented by the growth of viral misinformation, which contributes to create rumours and hoaxes around scientific threads. In order to avoid this kind of problems, www.action-euproject.eu is also designed to directly reach its audience even with social networks integration and with newsletters.


Informatics is the discipline that studies the information processing through automated elaborations. The term appears for the first time in 1957, and since that time Computer Science has grown, reaching an unthinkable evolution, so that the common devices we use in our everyday lives (personal computers, notebooks, tablets, smartphones) are more powerful than the NASA calculators at the time of moon\’s landing. This evolution leads to privacy and security matters: our devices process everyday an important number of sensitive data, and are everyday exposed to the risks of computer security.

This website has been designed following usability guidelines, with a logical sitemap, an easy system of options, a clear graphic style, a responsive graphic template and a robust Content Management System, in order to ensure the website security and a rigid privacy policy.

Complete Article

}, keywords = {computer security, misinformation, privacy, scientific dissemination, usability, Website}, doi = {10.7363/040254}, url = {http://www.jpnim.com/index.php/jpnim/article/view/040254}, author = {Matteo Mauri} }