Schizophrenia (SCZ) is a debilitating neuropsychiatric syndrome with typical onset during the second decade of life, and characterized by pronounced deficits in sensory and cognitive processing1. Hypotheses regarding its neurodevelopmental origins date back to Kraepelin, and later studies of high-risk children describe neurological “dysmaturation” during early childhood2. Genetic risk for SCZ, as measured by polygenic risk scores (PRS), and brain functional connectivity have been studied among those affected with SCZ3–5. However, investigating neurodevelopmental patterns of connectivity in unaffected adolescents and young adults, at varying levels of polygenic susceptibility, may uncover basic patterns of brain connectivity that could underlie development of the disorder. This information can elucidate basic neurobiological mechanisms by which the variants that contribute to genetic risk for SCZ affect brain connectivity and development patterns.
