@article {459, title = {Genome-wide analyses of individual differences in quantitatively assessed reading- and language-related skills in up to 34,000 people}, journal = {Proceedings of the National Academy of Sciences (PNAS)}, volume = {119}, year = {2022}, pages = {e2202764119}, abstract = {

The use of spoken and written language is a fundamental human capacity. Individual differences in reading- and language-related skills are influenced by genetic variation, with twin-based heritability estimates of 30 to 80\% depending on the trait. The genetic architecture is complex, heterogeneous, and multifactorial, but investigations of contributions of single-nucleotide polymorphisms (SNPs) were thus far underpowered. We present a multicohort genome-wide association study (GWAS) of five traits assessed individually using psychometric measures (word reading, nonword reading, spelling, phoneme awareness, and nonword repetition) in samples of 13,633 to 33,959 participants aged 5 to 26 y. We identified genome-wide significant association with word reading (rs11208009, P = 1.098 \× 10\−8) at a locus that has not been associated with intelligence or educational attainment. All five reading-/language-related traits showed robust SNP heritability, accounting for 13 to 26\% of trait variability. Genomic structural equation modeling revealed a shared genetic factor explaining most of the variation in word/nonword reading, spelling, and phoneme awareness, which only partially overlapped with genetic variation contributing to nonword repetition, intelligence, and educational attainment. A multivariate GWAS of word/nonword reading, spelling, and phoneme awareness maximized power for follow-up investigation. Genetic correlation analysis with neuroimaging traits identified an association with the surface area of the banks of the left superior temporal sulcus, a brain region linked to the processing of spoken and written language. Heritability was enriched for genomic elements regulating gene expression in the fetal brain and in chromosomal regions that are depleted of Neanderthal variants. Together, these results provide avenues for deciphering the biological underpinnings of uniquely human traits.

}, keywords = {genome-wide association study, language, meta-analysis, reading}, doi = {10.1073/pnas.2202764119}, author = {Eising, Else and Mirza-Schreiber, Nazanin and de Zeeuw, Eveline L and Wang, Carol A and Truong, Dongnhu T and Allegrini, Andrea G and Shapland, Chin Yang and Zhu, Gu and Wigg, Karen G and Gerritse, Margot L and Molz, Barbara and Alag{\"o}z, G{\"o}kberk and Gialluisi, Alessandro and Abbondanza, Filippo and Rimfeld, Kaili and van Donkelaar, Marjolein and Liao, Zhijie and Jansen, Philip R and Andlauer, Till F M and Bates, Timothy C and Bernard, Manon and Blokland, Kirsten and Bonte, Milene and B{\o}rglum, Anders D and Bourgeron, Thomas and Brandeis, Daniel and Ceroni, Fabiola and Cs{\'e}pe, Val{\'e}ria and Dale, Philip S and de Jong, Peter F and DeFries, John C and D{\'e}monet, Jean-Fran\c cois and Demontis, Ditte and Feng, Yu and Gordon, Scott D and Guger, Sharon L and Hayiou-Thomas, Marianna E and Hern{\'a}ndez-Cabrera, Juan A and Hottenga, Jouke-Jan and Hulme, Charles and Kere, Juha and Kerr, Elizabeth N and Koomar, Tanner and Landerl, Karin and Leonard, Gabriel T and Lovett, Maureen W and Lyytinen, Heikki and Martin, Nicholas G and Martinelli, Angela and Maurer, Urs and Michaelson, Jacob J and Moll, Kristina and Monaco, Anthony P and Morgan, Angela T and N{\"o}then, Markus M and Pausova, Zdenka and Pennell, Craig E and Pennington, Bruce F and Price, Kaitlyn M and Rajagopal, Veera M and Ramus, Franck and Richer, Louis and Simpson, Nuala H and Smith, Shelley D and Snowling, Margaret J and Stein, John and Strug, Lisa J and Talcott, Joel B and Tiemeier, Henning and van der Schroeff, Marc P and Verhoef, Ellen and Watkins, Kate E and Wilkinson, Margaret and Wright, Margaret J and Barr, Cathy L and Boomsma, Dorret I and Carreiras, Manuel and Franken, Marie-Christine J and Gruen, Jeffrey R and Luciano, Michelle and M{\"u}ller-Myhsok, Bertram and Newbury, Dianne F and Olson, Richard K and Paracchini, Silvia and Paus, Tom{\'a}\v s and Plomin, Robert and Reilly, Sheena and Schulte-K{\"o}rne, Gerd and Tomblin, J Bruce and van Bergen, Elsje and Whitehouse, Andrew J O and Willcutt, Erik G and St Pourcain, Beate and Francks, Clyde and Fisher, Simon E} } @article {435, title = {Investigating the genetic architecture of noncognitive skills using GWAS-by-subtraction}, journal = {Nature Genetics}, volume = {53}, year = {2021}, pages = {35{\textendash}44}, abstract = {

Little is known about the genetic architecture of traits affecting educational attainment other than cognitive ability. We used genomic structural equation modeling and prior genome-wide association studies (GWASs) of educational attainment (n = 1,131,881) and cognitive test performance (n = 257,841) to estimate SNP associations with educational attainment variation that is independent of cognitive ability. We identified 157 genome-wide-significant loci and a polygenic architecture accounting for 57\% of genetic variance in educational attainment. Noncognitive genetics were enriched in the same brain tissues and cell types as cognitive performance, but showed different associations with gray-matter brain volumes. Noncognitive genetics were further distinguished by associations with personality traits, less risky behavior and increased risk for certain psychiatric disorders. For socioeconomic success and longevity, noncognitive and cognitive-performance genetics demonstrated associations of similar magnitude. By conducting a GWAS of a phenotype that was not directly measured, we offer a view of genetic architecture of noncognitive skills influencing educational success.

}, doi = {10.1038/s41588-020-00754-2}, author = {Demange, Perline A and Malanchini, Margherita and Mallard, Travis T and Biroli, Pietro and Cox, Simon R and Grotzinger, Andrew D and Tucker-Drob, Elliot M and Abdellaoui, Abdel and Arseneault, Louise and van Bergen, Elsje and Boomsma, Dorret I and Caspi, Avshalom and Corcoran, David L and Domingue, Benjamin W and Harris, Kathleen Mullan and Ip, Hill F and Mitchell, Colter and Moffitt, Terrie E and Poulton, Richie and Prinz, Joseph A and Sugden, Karen and Wertz, Jasmin and Williams, Benjamin S and de Zeeuw, Eveline L and Belsky, Daniel W and Harden, K Paige and Nivard, Michel G} } @article {451, title = {Parental age in relation to offspring{\textquoteright}s neurodevelopment}, journal = {Journal of Clinical Child \& Adolescent Psychology}, volume = {50}, year = {2021}, pages = {632{\textendash}644}, abstract = {

Objective: Advanced parenthood increases the risk of severe neurodevelopmental disorders like autism, Down syndrome and schizophrenia. Does advanced parenthood also negatively impact offspring\&$\#$39;s general neurodevelopment?

Method: We analyzed child-, father-, mother- and teacher-rated attention-problems (N = 38,024), and standardized measures of intelligence (N = 10,273) and educational achievement (N = 17,522) of children from four Dutch population-based cohorts. The mean age over cohorts varied from 9.73-13.03. Most participants were of Dutch origin, ranging from 58.7\%-96.7\% over cohorts. We analyzed 50\% of the data to generate hypotheses and the other 50\% to evaluate support for these hypotheses. We aggregated the results over cohorts with Bayesian research synthesis.

Results: We mostly found negative linear relations between parental age and attention-problems, meaning that offspring of younger parents tended to have more attention problems. Maternal age was positively and linearly related to offspring\&$\#$39;s IQ and educational achievement. Paternal age showed an attenuating positive relation with educational achievement and an inverted U-shape relation with IQ, with offspring of younger and older fathers at a disadvantage. Only the associations with maternal age remained after including SES. The inclusion of child gender in the model did not affect the relation between parental age and the study outcomes.

Conclusions: Effects were small but significant, with better outcomes for children born to older parents. Older parents tended to be of higher SES. Indeed, the positive relation between parental age and offspring neurodevelopmental outcomes was partly confounded by SES.

}, doi = {10.1080/15374416.2020.1756298}, author = {Veldkamp, S A M and Zondervan-Zwijnenburg, M A J and van Bergen, Elsje and Barzeva, S A and Tamayo-Martinez, N and Becht, A I and van Beijsterveldt, C E M and Meeus, W and Branje, S and Hillegers, M H J and Oldehinkel, A J and Hoijtink, H J A and Boomsma, D I and Hartman, C} } @article {418, title = {Genetic and environmental influences on different forms of bullying perpetration, bullying victimization, and their co-occurrence}, journal = {Behavior Genetics}, volume = {49}, year = {2019}, pages = {432{\textendash}443}, abstract = {

Bullying comes in different forms, yet most previous genetically-sensitive studies have not distinguished between them. Given the serious consequences and the high prevalence of bullying, it is remarkable that the aetiology of bullying and its different forms has been under-researched. We present the first study to investigate the genetic architecture of bullying perpetration, bullying victimization, and their co-occurrence for verbal, physical and relational bullying. Primary-school teachers rated 8215 twin children on bullying perpetration and bullying victimization. For each form of bullying, we investigated, through genetic structural equation modelling, the genetic and environmental influences on being a bully, a victim or both. 34\% of the children were involved as bully, victim, or both. The correlation between being a bully and being a victim varied from 0.59 (relational) to 0.85 (physical). Heritability was \  70\% for perpetration and \  65\% for victimization, similar in girls and boys, yet both were somewhat lower for the relational form. Shared environmental influences were modest and more pronounced among girls. The correlation between being a bully and being a victim was explained mostly by genetic factors for verbal (\  71\%) and especially physical (\  77\%) and mostly by environmental factors for relational perpetration and victimization (\  60\%). Genes play a large role in explaining which children are at high risk of being a victim, bully, or both. For victimization this suggests an evocative gene-environment correlation: some children are at risk of being exposed to bullying, partly due to genetically influenced traits. So, genetic influences make some children more vulnerable to become a bully, victim or both.

}, keywords = {Bully-victims, Bullying, heritability, School, twins, Victimization}, doi = {10.1007/s10519-019-09968-5}, author = {Veldkamp, Sabine A M and Boomsma, Dorret I and de Zeeuw, Eveline L and van Beijsterveldt, Catharina E M and Bartels, Meike and Dolan, Conor V and van Bergen, Elsje} } @article {414, title = {The Netherlands Twin Register: Longitudinal research based on twin and twin-family designs}, journal = {Twin Research and Human Genetics}, volume = {22}, year = {2019}, pages = {623{\textendash}636}, abstract = {

The Netherlands Twin Register (NTR) is a national register in which twins, multiples and their parents, siblings, spouses and other family members participate. Here we describe the NTR resources that were created from more than 30 years of data collections; the development and maintenance of the newly developed database systems, and the possibilities these resources create for future research. Since the early 1980s, the NTR has enrolled around 120,000 twins and a roughly equal number of their relatives. The majority of twin families have participated in survey studies, and subsamples took part in biomaterial collection (e.g., DNA) and dedicated projects, for example, for neuropsychological, biomarker and behavioral traits. The recruitment into the NTR is all inclusive without any restrictions on enrollment. These resources - the longitudinal phenotyping, the extended pedigree structures and the multigeneration genotyping - allow for future twin-family research that will contribute to gene discovery, causality modeling, and studies of genetic and cultural inheritance.

}, keywords = {biobank, endophenotyping, longitudinal phenotyping, multigeneration pedigree, twins, zygosity}, doi = {10.1017/thg.2019.93}, author = {Ligthart, Lannie and van Beijsterveldt, Catharina E M and Kevenaar, Sofieke T and de Zeeuw, Eveline and van Bergen, Elsje and Bruins, Susanne and Pool, Ren{\'e} and Helmer, Quinta and van Dongen, Jenny and Hottenga, Jouke-Jan and Van{\textquoteright}t Ent, Dennis and Dolan, Conor V and Davies, Gareth E and Ehli, Erik A and Bartels, Meike and Willemsen, Gonneke and de Geus, Eco J C and Boomsma, Dorret I} } @article {403, title = {Why do children read more? The influence of reading ability on voluntary reading practices}, journal = {Journal of Child Psychology and Psychiatry}, volume = {59}, year = {2018}, pages = {1205{\textendash}1214}, abstract = {

BACKGROUND: This study investigates the causal relationships between reading and print exposure and investigates whether the amount children read outside school determines how well they read, or vice versa. Previous findings from behavioural studies suggest that reading predicts print exposure. Here, we use twin-data and apply the behaviour-genetic approach of direction of causality modelling, suggested by Heath et al. (), to investigate the causal relationships between these two traits.

METHOD: Partial data were available for a large sample of twin children (N = 11,559) and 262 siblings, all enrolled in the Netherlands Twin Register. Children were assessed around 7.5 years of age. Mothers completed questionnaires reporting children\&$\#$39;s time spent on reading activities and reading ability. Additional information on reading ability was available through teacher ratings and performance on national reading tests. For siblings reading test, results were available.

RESULTS: The reading ability of the twins was comparable to that of the siblings and national norms, showing that twin findings can be generalized to the population. A measurement model was specified with two latent variables, Reading Ability and Print Exposure, which correlated .41. Heritability analyses showed that Reading Ability was highly heritable, while genetic and environmental influences were equally important for Print Exposure. We exploited the fact that the two constructs differ in genetic architecture and fitted direction of causality models. The results supported a causal relationship running from Reading Ability to Print Exposure.

CONCLUSIONS: How much and how well children read are moderately correlated. Individual differences in print exposure are less heritable than individual differences in reading ability. Importantly, the present results suggest that it is the children\&$\#$39;s reading ability that determines how much they choose to read, rather than vice versa.

}, keywords = {behaviour-genetics, causal modelling, Direction of causality models, print exposure, reading skills, twin studies}, doi = {10.1111/jcpp.12910}, author = {van Bergen, Elsje and Snowling, Margaret J and de Zeeuw, Eveline L and van Beijsterveldt, Catharina E M and Dolan, Conor V and Boomsma, Dorret I} }