Ulrika Ådén

Preterm birth occurs in 6-12% of pregnancies globally. Intensive care of preterm infants has made major advance over the last decades resulting in dramatically increased survival rates for the most immature infants and a whole new generation of children entering school. While incidence of cerebral palsy decrease, the incidence of neurodevelopmental disorders including intellectual dysfunction, ADHD and autism spectrum disorder now increase and risks are related to immaturity at birth. In children born before 28 weeks´ gestation, two thirds eventually have neurodevelopmental impairments affecting their daily life and academic achievements. To improve outcomes, there is a need for identifying early signs of adverse brain development and to find effective early interventions.The overarching aim is to examine the relations between modifiable perinatal risks, family risk, brain development, neurodevelopment and neurodevelopmental outcomes in children born extremely preterm to improve early prediction and outcomes. In a randomized controlled study, we coach parents to support their preterm born infant´s development in the first year of life and then evaluate neurodevelopmental outcomes. Based on the study results and prediction models we plan to further individualize the intervention.

Autism Spectrum Disorder (ASD) risk is primarily of genetic origins. One source through which environmental effects may be influential is preterm birth (PTB

birth &lt

37 weeks gestation) which constitutes 6% of all births in Sweden (10% world wide). PTB is primarily of environmental origin, due to disease in the pregnant woman or her fetus. The processes underlying PTB may initiate ASD. This hypothesis has not been previously studied. If true, the heritability of ASD may be much lower in PTB children suggesting that PTB defines a subset of the general population where environmental risk play the major role for ASD risk.The goal of our project is to examine the ASD-etiology in PTB children and test if the etiology is different compared to term-born

identify risk factors for ASD in PTB children, and to estimate the public health consequences of these factors.We will create a cohort of all Swedish children born 1995-2014 using the national registers, replicate results in Finland and examine genetic markers in a Swedish genetic sample.Aims are: (1) Determine the epidemiology and risk factors for ASD in PTB children. (2) Test if the risk factors in aim 1 are due to confounding, and estimate their public health consequences. (3) Compare ASD susceptibility in PTB and term-born children using both family data and molecular genetic data. (4) Explore potentials for risk prediction in a clinical cohortThis will be the most systematic investigation ASD-etiology in PTB children to date.