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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: 20 October 2024 | Viewed by 2131

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 (2 papers)

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Research

15 pages, 1571 KiB  
Article
Moderate Prenatal Alcohol Exposure Increases Toll-like Receptor Activity in Umbilical Cord Blood at Birth: A Pilot Study
by Jessie R. Maxwell, Shahani Noor, Nathaniel Pavlik, Dominique E. Rodriguez, Lidia Enriquez Marquez, Jared DiDomenico, Sarah J. Blossom and Ludmila N. Bakhireva
Int. J. Mol. Sci. 2024, 25(13), 7019; https://doi.org/10.3390/ijms25137019 - 27 Jun 2024
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Abstract
The prevalence of prenatal alcohol exposure (PAE) is increasing, with evidence suggesting that PAE is linked to an increased risk of infections. PAE is hypothesized to affect the innate immune system, which identifies pathogens through pattern recognition receptors, of which toll-like receptors (TLRs) [...] Read more.
The prevalence of prenatal alcohol exposure (PAE) is increasing, with evidence suggesting that PAE is linked to an increased risk of infections. PAE is hypothesized to affect the innate immune system, which identifies pathogens through pattern recognition receptors, of which toll-like receptors (TLRs) are key components. We hypothesized that light-to-moderate PAE would impair immune responses, as measured by a heightened response in cytokine levels following TLR stimulation. Umbilical cord samples (10 controls and 8 PAE) from a subset of the Ethanol, Neurodevelopment, Infant and Child Health Study-2 cohort were included. Peripheral blood mononuclear cells (PMBCs) were stimulated with one agonist (TLR2, TLR3, TLR4, or TLR9). TLR2 agonist stimulation significantly increased pro-inflammatory interleukin-1-beta in the PAE group after 24 h. Pro- and anti-inflammatory cytokines were increased following stimulation with the TLR2 agonists. Stimulation with TLR3 or TLR9 agonists displayed minimal impact overall, but there were significant increases in the percent change of the control compared to PAE after 24 h. The results of this pilot investigation support further work into the impact on TLR2 and TLR4 response following PAE to delineate if alterations in levels of pro- and anti-inflammatory cytokines have clinical significance that could be used in patient management and/or attention to follow-up. Full article
(This article belongs to the Special Issue Neonatal Neurodevelopmental Toxicology)
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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
Cited by 1 | Viewed by 1247
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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