Delineating the Transmission of Subthreshold Psychosis Symptoms Across Generations: The Philadelphia Family Neurodevelopmental Cohort

阐明亚临床精神病症状的代际传递:费城家族神经发育队列研究

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Abstract

BACKGROUND AND HYPOTHESIS: Intergenerational factors are implicated in development of schizophrenia spectrum disorders. Studying psychosis spectrum (PS) symptoms dimensionally in a longitudinal, prospective intergenerational cohort can provide crucial insight into risk pathways. Thus, we established the Philadelphia Family Neurodevelopmental Cohort (PFNC), an intergenerational study that follows Philadelphia Neurodevelopmental Cohort (PNC) participants as they transition to parenthood, along with their offspring. This first report describes the creation of the PFNC, followed by an examination of longitudinal associations between risk factors assessed in adolescence (PS symptoms, cognition, and traumatic life events) and mental health and resilience outcomes in parenthood. STUDY DESIGN: Since the PNC was accrued (2009-2011; ages 8-21 years), many participants have become parents. As an initial step in the development of PFNC, participants completed a virtual self-report battery to assess parental status, family structure, current mental health symptoms, and parent-relevant risk and resilience factors. STUDY RESULTS: The current PFNC includes 456 PNC participants with 740 offspring, consisting primarily of biological mothers (female = 84%; Black = 65%; mean parent age = 28.38 years, SD = 3.40; mean offspring age = 4.01 years, SD = 3.36). Findings revealed adolescent PS symptoms and traumatic events are associated with PS symptoms in parenthood. Adolescent PS symptoms were also linked to higher levels of household chaos approximately 12 years later. CONCLUSION: Despite the growing recognition of the intergenerational transmission of neuropsychiatric risk, there is limited research examining intergenerational risk factors in the context of PS symptoms. The PFNC represents a critical next step toward advancing our understanding of intergenerational pathways contributing to PS risk.

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