Psychotic-like experiences (PLEs) include experiences such as hallucinations and
delusional thinking that can occur in the absence of a clinical disorder. PLEs peak
in middle childhood but appear to spontaneously remit in most children. Nevertheless,
their presence, and particularly their persistence, are associated with an
increased risk of developing later psychosis and poor psychiatric and social outcomes.
However, the mechanisms by which they are generated during childhood
are unclear. Existing models of psychosis cite early life experience and childhood
neurodevelopment as important but often examine these retrospectively. Furthermore,
they suggest mechanisms for how psychotic experiences are generated that
are assumed to apply across the lifespan. This assumption has remained untested,
however. Consequently, in this thesis, I investigated neurocognitive mechanisms
of PLEs in 9-10 year-old-children using data from the Adolescent Brain Cognitive
Development (ABCD) study. In Study 1, I examined whether the established mechanistic
risk factors in adult psychosis – affective symptoms, traumatic experiences,
cognitive function, structural brain changes – are associated with PLEs using network
analysis, finding only that depression-related symptoms were associated with
PLEs. In Study 2, I tested whether fMRI activation in striatal reward pathways was
associated with PLEs in children, as this is an established finding in adults. This
study found no strong evidence for alteration to striatal reward pathways with a
high likelihood that it was absent, rather than undetectable. Given the prognostic
and aetiological important of persistence of PLEs, in Study 3, I tested affective,
trauma-related, cognitive and striatal reward activation predictors of 1-year PLE
persistence. Only depressive symptoms were substantial predictors. Depressive
symptoms emerged as the strongest predictor of PLEs at this developmental stage,
both cross-sectionally and longitudinally. The findings indicate that PLEs in childhood
are not a ‘mini psychosis syndrome’ and developmental-stage specific models
of psychotic experiences in children are required.