Background And Aims: Prenatal fine particulate matter (PM) exposure has been linked to adverse neurodevelopment. However, epidemiological evidence remains inconclusive and little information about the effects of various PM components on child neurodevelopment is currently known. The underlying mechanism was also not elucidated. The study aimed to evaluate the effects of PM and components exposure on child neurodevelopmental delays and the role of placental small extracellular vesicles (sEVs)-derived miRNAs in the associations.
Methods: We included 267 mother-child pairs in this analysis. Prenatal PM and components (i.e. elements, water-soluble ions, and PAHs) exposure during three trimesters were monitored through personal PM sampling. Child neurodevelopment at 2, 6, and 12 months old were evaluated by Ages and Stages Questionnaire (ASQ). We isolated sEVs from placental tissue to analyze the change of sEVs-derived miRNAs in response to PM. Associations between the PM-associated miRNAs and child neurodevelopment were evaluated using multivariate linear regression models.
Results: The PM exposure levels in the three trimesters range from 2.51 to 185.21 μg/m. Prenatal PM and the components of Pb, Al, V and Ti exposure in the second and third trimester were related to decreased ASQ scores communication, problem-solving and personal-social domains in children aged 2 or 6 months. RNA sequencing identified fifteen differentially expressed miRNAs. The miR-101-3p and miR-520d-5p were negatively associated with PM and Pb component. miR-320a-3p expression was positively associated with PM and V component. Meanwhile, the miR-320a-3p was associated with decreased ASQ scores, as reflected by ASQ-T (β: -2.154, 95 % CI: -4.313, -0.516) and problem-solving domain (β: -0.605, 95 % CI: -1.111, -0.099) in children aged 6 months.
Conclusion: Prenatal exposure to PM and its Pb, Al, V & Ti component were associated with infant neurodevelopmental delays. The placenta sEVs derived miRNAs, especially miR-320a-3p, might contribute to an increased risk of neurodevelopmental delays.
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http://dx.doi.org/10.1016/j.scitotenv.2022.156747 | DOI Listing |
J Pediatr
January 2025
Department of Acute Febrile Illnesses, Evandro Chagas National Institute of Infectious Diseases, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.
Objective: To investigate the effects of intrauterine and perinatal exposure to chikungunya virus (CHIKV) on neurodevelopment in infants and toddlers.
Study Design: We conducted a cohort study comparing children with intrauterine or perinatal exposure to maternal CHIKV infection with unexposed controls in Rio de Janeiro, Brazil. Neurodevelopment was assessed with General Movement Assessments (GMA) in the first six months of life, and the Bayley-III Scales of Infant and Toddler Development and Modified Checklist for Autism in Toddlers (M-CHAT) for older children.
Pediatr Neurol
January 2025
Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Background: To explore the utility of general movements assessment as a predictive tool of the neurological outcome in term-born infants with hypoxic-ischemic encephalopathy (HIE) at ages six and 12 months.
Methods: This prospective observational study was conducted for 18 months (August 2018 to December 2019). Term-born newborns with HIE were included.
Cell Rep
January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
View Article and Find Full Text PDFNutrients
January 2025
Department of Psychiatry and Behavioral Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Background/objectives: While studies in rat pups suggest that early zinc exposure is critical for optimal brain structure and function, associations of prenatal zinc intake with measures of brain development in infants are unknown. This study aimed to assess the associations of maternal zinc intake during pregnancy with MRI measures of brain tissue microstructure and neurodevelopmental outcomes, as well as to determine whether MRI measures of the brain mediated the relationship between maternal zinc intake and neurodevelopmental indices.
Methods: Forty-one adolescent mothers were recruited for a longitudinal study during pregnancy.
Nutrients
January 2025
Department of Maternal and Child Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.
: We aimed to identify neonatal circulating metabolic alterations associated with maternal gestational diabetes mellitus (GDM) and to explore whether these altered metabolites could mediate the association of GDM with offspring neurodevelopment. Additionally, we investigated whether neonatal circulating metabolites could improve the prediction of offspring neurodevelopmental disorders over traditional risk factors. : The retrospective cohort study enrolled 1228 mother-child dyads in South China.
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