Neurotoxicology and teratology最新文献

Background: Exposure to maternal stress and depression during pregnancy can have a marked impact on birth outcomes and child development, escalating the likelihood of preterm birth, lower birth weight, and various domains of physical and neurodevelopment.

Methods: The joint ECHO.CA.IL cohort is comprised of the Chemicals in Our Bodies (CIOB) and Illinois Kids Development Study (IKIDS) prospective cohorts, recruiting pregnant women in San Francisco, CA, and Urbana-Champaign, IL, respectively. Using a combined sample of 428 mother-infant dyads, we examined associations between two prenatal measures of maternal stress (perceived stress (PSS) and stressful events (SLE)), as well as maternal depression, and five domains of neurodevelopment via the Ages & Stages Questionnaire (ASQ) administered at 7.5 months. Linear regression models were adjusted for relevant demographic characteristics and used to identify patterns of association.

Results: CIOB mothers were comparatively racially/ethnically diverse (52 % white, 28 % Asian American/Pacific Islander, 12 % Hispanic), while IKIDS mothers were disproportionately white (80 %). Both cohorts demonstrated high levels of maternal education and were similar in terms of other demographic characteristics. CIOB mothers reported higher levels of stress (e.g.

, sle: 49.63 % report ≥1 event) compared to IKIDS mothers (e.g.

, sle: 16.34 % report ≥1 event). In adjusted linear models, patterns of association were nearly uniformly negative between stress and ASQ measures, with associations between PSS and fine motor skills (β-0.26, CI = -0.52; 0.00) and SLEs and communication skills (β = -2.9245, CI = -6.1643; 0.3152) showing the strongest associations (p < 0.1). Depression showed no significant or clear pattern of association with ASQ scores.

Conclusion: This study found negative associations between prenatal maternal stress and infant neurodevelopment in the combined ECHO.CA.IL cohort, suggesting that prenatal stress is associated with delayed development of motor and communication skills during infancy. The inconclusive links between maternal depression and ASQ outcomes leave open the question regarding the influence of prenatal depression on early child neurodevelopment.

Exposure to psychosocial stress during pregnancy has been associated with the emergence of neurodevelopmental and neuropsychiatric disorders in offspring. The placenta is known to orchestrate various functions that are essential for normal fetal development, including the brain. It has therefore been postulated that alterations in such functions, and downstream signaling, have the potential to dramatically affect brain developmental trajectories and contribute to adverse neurodevelopmental outcomes. This review will focus on discussing various placental functions that have been proposed to be affected by exposure to prenatal psychosocial stress and the implications of such disruptions on long-term neurodevelopmental programming.

Evolutionary-developmental theories propose that early adverse experiences adaptively shift the timing (i.e., onset) and tempo (i.e., rate) of pubertal maturation. Empirical evidence of links between early life adversity and pubertal maturation is mixed, potentially in part because isolating the unique impacts of early environments is challenging. The current accelerated longitudinal study used a quasi-experimental design to examine pubertal maturation among 132 previously-institutionalized (PI), internationally adopted children who experienced a time-limited form of severe early life adversity, compared to 169 non-adopted (NA) children. Based on prior literature, we also assessed whether pubertal timing and/or tempo are pathways by which early adversity relates to later symptoms of psychopathology. At each of three annual sessions, Tanner pubertal staging was determined by nurse exam, and symptoms of psychopathology were captured in a composite of child self-reported internalizing and parent-reported externalizing symptoms. Findings revealed that, only among children at Tanner pubertal stages 3 or below, PI children were more likely to have reached stage 3 compared to NA children, reflective of earlier pubertal timing. No group differences were found for pubertal tempo. In the subsample of children at Tanner stage 3 or lower, earlier pubertal timing was an indirect pathway by which early adversity related to both higher levels and greater longitudinal declines in internalizing and externalizing symptoms of psychopathology, accounting for a small proportion of the total effect of early adversity on psychopathology. Results from this quasi-experimental study add to existing research on associations between early adversity, early pubertal timing, and psychopathology, further suggesting that links may be specific to timing but not tempo. While findings broadly align with recent calls to consider early pubertal maturation as a transdiagnostic risk marker with utility for identifying children who could benefit from early mental health intervention, they also suggest that pubertal timing is unlikely to be a robust target for reducing psychopathology risk in these children.

Objective: Though caffeine use during pregnancy is common, its longitudinal associations with child behavioral and physical health outcomes remain poorly understood. Here, we estimated associations between prenatal caffeine exposure, body mass index (BMI), and behavior as children enter adolescence.

Method: Longitudinal data and caregiver-reported prenatal caffeine exposure were obtained from the ongoing Adolescent Brain and Cognitive Development (ABCD)^SM Study, which recruited 11,875 children aged 9-11 years at baseline from 21 sites across the United States starting June 1, 2016. Prenatal caffeine exposure was analyzed as a 4-level categorical variable, and further group contrasts were used to characterize "any exposure" and "daily exposure" groups. Outcomes included psychopathology characteristics in children, sleep problems, and BMI. Potentially confounding covariates included familial (e.g., income, familial psychopathology), pregnancy (e.g., prenatal substance exposure), and child (e.g., caffeine use) variables.

Results: Among 10,873 children (5686 boys [52.3 %]; mean [SD] age, 9.9 [0.6] years) with nonmissing prenatal caffeine exposure data, 6560 (60 %) were exposed to caffeine prenatally. Relative to no exposure, daily caffeine exposure was associated with higher child BMI (β = 0.08; FDR-corrected p = 0.02), but was not associated with child behavior following correction for multiple testing. Those exposed to two or more cups of caffeine daily (n = 1028) had greater sleep problems than those with lower/no exposure (β > 0.92; FDR-corrected p < 0.04).

Conclusion: Daily prenatal caffeine exposure is associated with heightened childhood BMI, and when used multiple times a day greater sleep problems even after accounting for potential confounds. Whether this relationship is a consequence of prenatal caffeine exposure or its correlated factors remains unknown.

Developmental chronic low-level lead (Pb) exposure disrupts central nervous system function and diminishes neurocognition. Microglial cell activation might contribute to these deficits. The present study evaluated the effects of developmental sub-chronic low-level lead exposure on microglial cells and the possible effectiveness of a natural anti-inflammatory intervention with apigenin to mitigate these effects. From PND 0 to 28, 87 C57BL/6 J mice were exposed to one of six treatment conditions: 0 ppm Pb; 30 ppm Pb; 430 ppm Pb; 30 ppm Pb + 400 ppm apigenin; 430 ppm Pb + 400 ppm apigenin; or 400 ppm apigenin, via dams' drinking water. Following sacrifice, brain tissue was harvested and microglial cells were labeled via immunohistochemistry and counted within the dentate gyrus (DG) using unbiased stereology methods. It was hypothesized that developmental sub-chronic low-level lead exposure would increase microglial cell numbers within the DG and that apigenin treatment may mitigate these effects. A significant effect of treatment group was found and post-hoc analyses revealed that Pb-exposure generated an increased number of microglial cells as compared to controls. Interestingly, the 30 ppm Pb with apigenin treatment group did not generate microglial cell numbers different from the control group unexposed to Pb. These results suggested that developmental sub-chronic low-level lead exposure increased microglial cell activation within the DG and that, at low-levels of Pb exposure, apigenin treatment may mitigate these effects. These results provided the groundwork for studies that could identify an effective intervention to alleviate the effects of developmental chronic low-level lead exposure in child neurocognition.