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Neonatal Neurodevelopmental Toxicology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1077

Special Issue Editor


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Guest Editor
Department of Pediatrics and Neurosciences, University of New Mexico, Albuquerque, NM 87131, USA
Interests: neurology; neuroscience

Special Issue Information

Dear Colleagues,

This Special Issue, “Neonatal Neurodevelopmental Toxicology”, aims to collect cutting-edge original research or in-depth review articles concerning exposures that occur during pregnancy or in the first few months of life that impact neurodevelopment. Infants remain vulnerable to insults during fetal development as well as during the neurological development that continues throughout early childhood. However, a better understanding of the impact of insults can also allow for new therapies and treatments to be pursued at a time when optimal outcomes can be achieved. Insults may include, but are not limited to, substance exposure, environmental exposures, chemical exposures, or other exposures backed up by research that supports their impact on neonatal neurodevelopment. Research and reviews should focus on describing the type of impact observed, provide evidence for alterations in specific molecular mechanisms when possible, and provide possible agents and/or therapies that may ameliorate any negative impacts if known. As IJMS focuses on molecular science, any clinical submissions should include biomolecular experiments in order to be considered for publication.

Dr. Jessie R. Maxwell
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Published Papers (1 paper)

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Research

21 pages, 3046 KiB  
Article
Independent and Combined Effects of Prenatal Alcohol Exposure and Prenatal Stress on Fetal HPA Axis Development
by Ludmila N. Bakhireva, Elizabeth Solomon, Melissa H. Roberts, Xingya Ma, Rajani Rai, Alexandria Wiesel, Sandra W. Jacobson, Joanne Weinberg and Erin D. Milligan
Int. J. Mol. Sci. 2024, 25(5), 2690; https://doi.org/10.3390/ijms25052690 - 26 Feb 2024
Viewed by 790
Abstract
Prenatal alcohol exposure (PAE) and prenatal stress (PS) are highly prevalent conditions known to affect fetal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The objectives of this study were to assess the effect of light PAE, PS, and PAE-PS interaction on fetal HPA axis [...] Read more.
Prenatal alcohol exposure (PAE) and prenatal stress (PS) are highly prevalent conditions known to affect fetal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The objectives of this study were to assess the effect of light PAE, PS, and PAE-PS interaction on fetal HPA axis activity assessed via placental and umbilical cord blood biomarkers. Participants of the ENRICH-2 cohort were recruited during the second trimester and classified into the PAE and unexposed control groups. PS was assessed by the Perceived Stress Scale. Placental tissue was collected promptly after delivery; gene and protein analysis for 11β-HSD1, 11β-HSD2, and pCRH were conducted by qPCR and ELISA, respectively. Umbilical cord blood was analyzed for cortisone and cortisol. Pearson correlation and multivariable linear regression examined the association of PAE and PS with HPA axis biomarkers. Mean alcohol consumption in the PAE group was ~2 drinks/week. Higher PS was observed in the PAE group (p < 0.01). In multivariable modeling, PS was associated with pCRH gene expression (β = 0.006, p < 0.01), while PAE was associated with 11β-HSD2 protein expression (β = 0.56, p < 0.01). A significant alcohol-by-stress interaction was observed with respect to 11β-HSD2 protein expression (p < 0.01). Results indicate that PAE and PS may independently and in combination affect fetal programming of the HPA axis. Full article
(This article belongs to the Special Issue Neonatal Neurodevelopmental Toxicology)
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