Neurodevelopmental disorders (NDDs) are a group of highly heritable childhood-onset conditions characterized by impairments in developmental domains such as communication, social interaction, motor skills, cognition, activity and emotion (1). Common NDDs are attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). While schizophrenia is a psychiatric disorder typically diagnosed after puberty, the onset is commonly preceded by childhood neurodevelopmental impairment (2,3). Although ASD, ADHD and schizophrenia are categorically defined for clinical purposes, they can also be viewed as the extremes of continuous trait dimensions found in the general population (4,5).

A large body of observational studies suggest that having a child with an NDD is associated with poorer parent functioning, including depression, inter-parental discord and maladaptive parenting behavior (6-10). While such parental traits have been proposed to increase risk or exacerbate child NDD problems, important alternative explanations are shared familial factors (e.g., shared genetic risk for NDD) and reverse causation (e.g., child NDD problems evoking inter-parental discord) (8). Previous studies attempting to disentangle these alternative explanations have primarily relied on twin and adoption study designs (8,11), with findings suggesting that child NDD traits evoke maternal negative parenting behaviors and inter-parental discord. However, twin and adoption studies are generally limited by small samples and potential non-representativeness of twin and adoption families. Better understanding of the potential effects of NDDs on parent functioning is needed in order to improve interventions for children with NDDs and their families.

Genetic advances now allow for direct measurement of the genetic risk burden for NDDs in individuals from the general population. If raising a child with an NDD, such as ASD, affects parent functioning, then children’s genetic risk burden for ASD should contribute to explaining variance in parent functioning over and above the parents’ genetic risk burden for ASD.

In the present study, we will examine whether child genetic risk burden for ASD, ADHD and schizophrenia predicts parent functioning (mental health, relationship harmony, parenting) when adjusting for parental genetic risk burden. We will use family trio data from two population based pregnancy cohorts: the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort and the Norwegian Mother and Child Cohort (MoBa). Data from the two cohorts will be analysed separately, and the results may be meta-analysed.

References
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