Thank you Erica!

thank you

Last but definitely not least is our Neurodiverse Advisory Committee (NAC) consisting of autistic citizens and scientists. In partnership with autismtreeproject.org we have assembled the NAC to provide us with the stakeholders perspective on autism research!

We will also investigate how environmental factors influence clinical outcome of genes in ASD. Samples of many thousands are needed to identify G. Capturing the effects of GxE requires sample sizes of millions. Juicy preliminary data will be posted soon to medrxiv. It takes a village, come join us!

As a novel approach to causal inference, we will use collider effects to find genetic evidence to SUPPORT a causal role of environmental exposure. If E has a strong effect that is uncorrelated with G in the population, genes will explain LESS of the variance in the explosed group!

Our 2022 paper in NG illustrates one example: the observed association of parental age with ausism consists of a mixture of causal pathway E → de novo mutation → ASD; and noncausal pathway Parental age ← polygenic score → ASD

We will use a multi-pronged approach to causal inference using data on G and E in >2 million people, including association, MR and GxE exploring the interplay of exposures with rare and common variation that contributes to ASD, and we will rigorously evaluate rGE in family and population

THE major challenge in epidemiological studies of the environment in autism is the pervasive passive correlation of genes and environment (rGE) that happens in the population, also known horizontal pleiotropy. There are causal effects to be found, but we need to separate correlation from causation

Autism has a strong genetic basis, 100 genes have been identified and we e have multiple independent genetic predictors that have very strong signals in the population. If you are going do and epidemiological study of E, you need to account for G and GxE! pmc.ncbi.nlm.nih.gov/articles/PMC...