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Margolis, A. E.

Publications and source records attributed to Margolis, A. E..

2 recordsLinked to original sources

Postnatal maternal care moderates the effects of prenatal bisphenol exposure on offspring neurodevelopmental, behavioral, and transcriptomic outcomes

Bisphenols (BPs), including BPA and "BPA-free" structural analogs, are commonly used plasticizers that are present in many plastics and are known endocrine disrupting chemicals. Prenatal exposure to BPA has been associated with negative neurodevelopmental and behavioral outcomes in children and rodent models. Prenatal BPA exposure has also been shown to impair postnatal maternal care provisioning, which can also affect offspring neurodevelopment and behavior. However, there is limited knowledge regarding the biological effects of prenatal exposure to bisphenols other than BPA and the interplay between prenatal BP exposure and postnatal maternal care on adult behavior. The purpose of the current study was to determine the interactive impact of prenatal BP exposure and postnatal maternal care on neurodevelopment and behavior. Our findings suggest that the effects of prenatal BP exposure on eye-opening, adult attentional set shifting and anxiety-like behavior in the open field are dependent on maternal care in the first five days of life. Interestingly, maternal care might also attenuate the effects of prenatal BP exposure on eye opening and adult attentional set shifting. Finally, transcriptomic profiles in male and female medial prefrontal cortex and amygdala suggest that the interactive effects of prenatal BP exposure and postnatal maternal care converge on estrogen receptor signaling and are involved in biological processes related to gene expression and protein translation and synthesis. Overall, these findings indicate that postnatal maternal care plays a critical role in the expression of the effects of prenatal BP exposure on neurodevelopment and adult behavior. Understanding the underlying biological mechanisms involved might allow us to identify potential avenues to mitigate the adverse effects of prenatal BP exposure and improve health and well-being in human populations.

neuroscience↗

Relative Brain Age Is Associated with Socioeconomic Status and Anxiety/Depression Problems in Youth

Socioeconomic status (SES) has been linked to differences in brain structure and psychiatric risk across the lifespan. Despite many neuropsychiatric disorders emerging in childhood, few studies have examined the influence of SES on brain aging and psychopathology in youth. We re-analyzed relative brain age (RBA) data from the Healthy Brain Network to examine the influence of SES components (parent education, occupation, household income-to-needs ratio (INR), public assistance enrollment) on RBA. RBA was previously determined using covariation patterns for cortical morphology, white, and subcortical gray matter volumes without SES in predictive models. We also examined associations between RBA and psychiatric symptoms (child behavior checklist). Full case analysis included 470 youth (5-17 years; 61.3% male), self-identifying as White (55%), African American (15%), Hispanic (9%), or multiracial (17.2%). Mean household income was 3.95{+/-}2.33 (Mean{+/-}SD) times the federal poverty threshold. Multiple linear regression examined if 1) SES components associated with RBA, and 2) RBA associated with psychiatric symptoms. Models covaried for sex, scan location, and parent psychiatric diagnoses. RBA associated with public assistance (p = 0.03), parent occupation (p = 0.01), and parent psychiatric diagnosis (p = 0.01), but not with INR and parent education. Parent occupation (p = 0.02) and RBA (p = 0.04) associated with CBCL anxiety/depression scores. Components of SES associated with brain aging, underscoring the risk of omitting these factors in developmental brain research. Further, delayed brain aging was associated with low parental occupational prestige and child anxiety/depression scores, suggesting a possible biological pathway from SES to mental health risk.

neuroscience↗