Nancy Adler Seed Grants Program

Social determinants of health (SDOH) are known to affect childhood brain development. Recent data suggests that these effects of SDOH can be seen as early as in fetal life. However, it is unknown what domains of SDOH are critical to in utero development of different regions of the brain. To answer this question, Drs. George and Rauschecker will leverage the large institutional pre-existing database of fetal MRIs performed in normal fetuses and a deep-learning based pipeline for quantification of total and regional fetal brain volumes. From parental demographics, they will derive 3 different census-derived indices (social deprivation index, childhood opportunity index, and social vulnerability index) that capture various domains of SDOH and assess its effects on fetal brain volumes. The methods developed and tested in this study are scalable to multi-institution studies to study overarching national trends as well as regional variations without the need for prospective collection of SDOH metrics. Identification of socioeconomic factors that contribute to this early disparity in brain development will be crucial in informing public health policy and efforts to both mitigate deleterious exposure and identify targets for early intervention.

Social and behavioral determinants of health (SBDHs) have been found to predict psychosis conversion. This has generated enthusiasm for SBDH-focused interventions (e.g., trauma and family-focused therapies) to improve health equity and clinical outcomes. Yet, a crucial piece remains unclear, how do SBDHs “get under the skin” and influence psychosis. Converging evidence shows that SBDHs, such as trauma and stress, can trigger biological changes leading to premature maturation, as reflected by early puberty and biological aging.  Premature brain maturation (or brain aging), a common metric of biological aging, is observed in schizophrenia. Moreover, premature brain maturation predicts psychosis conversion in individuals at clinical high-risk for psychosis (CHR-P). One hypothesis is that SBDHs directly influence psychosis conversion. Another possibility is that premature brain maturation mediates (at least partially) the process through which SBDHs increases risk for psychosis conversion. This proposal aims to: 1) assess prevalence rates of SBDHs and 2) examine brain maturation as a candidate biological intermediary by which SBDHs increase conversion risk. Findings can inform development of targeted interventions that reduce psychosis conversion risk across the socio-demographically and clinically heterogeneous CHR-P population, who are likely to be exposed to SBDHs. Such targeted interventions, which can slow down premature maturation in children exposed to adversity have the potential to advance clinical care and public policies aimed at increasing health equity in CHR-P adolescents and young adults.