Hello, we are the Association for Child and Adolescent Mental Health, or ACAMH for short. Hello, my name is Sandra Machlitt-Northen, and I'm a PhD student in the Department of biological and experimental psychology at Queen Mary University, London. This short video is intended to give a very brief overview of a paper that my colleagues and I recently published in the Journal of Child Psychology and Psychiatry titled "Polygenic scores for schizophrenia and major depression associated with psychosocial risk factors in children, evidence of gene-environment correlation." Research suggests that schizophrenia and major depression are associated with both genetic and environmental risk factors. These are likely intertwined in complex ways through gene-environment correlation, which describes how an individual's genetic predisposition can influence the exposure to particular environments. The aim of our study was, firstly, to identify if established environmental risk factors for schizophrenia and major depression in childhood are correlated with a genetic risk of these disorders. This was measured with polygenic risk scores derived from published large genome-wide association studies. Secondly, we wanted to establish whether patterns of gene-environment correlation differ between schizophrenia and major depression, and thirdly, between two British cohorts that are 42 years apart, the Millennium Cohort Study and the 1958 National Child Development study. Given that we had the parental and child genotypes from the Millennium Cohort Study, we were able to distinguish between passive and evocative gene-environment correlation. Passive gene-environment correlation occurs when the biological parents pass on the genetic traits to their children whilst also providing a specific environmental context. On the other hand, evocative gene-environment correlation occurs when a genetic predisposition gives rise to a particular behavior that evokes a specific response from the environment. For our first aim, we found that the child polygenic risk for both disorders was correlated with several environmental risk factors in childhood, for example, lack of father's involvement in childcare for schizophrenia in the 1958 National Child Development study and several indicators of low socioeconomic status for major depression in both cohorts. Our analysis shows that more than half of our significant associations reflected passive gene-environment correlation whereby the parents not only provide the genotypes to their offspring, but also the home environments in which the children grow up in. For our second aim, we identified that gene-environment correlation was more pronounced for the polygenic risk score for major depression and less so for schizophrenia, suggesting that gene-environment correlation differs between the two disorders, which may be due to the fact that the polygenic scores of these disorders reflect largely different genes with only partial overlap between them. Finally, when comparing our findings between the Millennium Cohort Study and the 1958 National Child's Development Study, our findings suggest that while some gene-environment correlations were stable across generations, such as low socioeconomic status, others likely changed due to a societal and cultural changes over 40 years. In some, findings confirm the complex relationship between environmental and genetic risk for psychiatric disorders and emphasize the importance of considering gene-environment interplay regarding the role of long-established environmental risk factors in childhood. Thank you so much for watching this video abstract. If you would like to find out more about our study, please feel free to read our full paper on the Journal of Child Psychology and Psychiatry website. Thank you. Find out more about becoming an ACAMH member, and to be part of the advancement of child and adolescent mental health, visit www.acamh.org.