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Brain Sciences
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Recent Advances in Fetal Alcohol Spectrum Disorder (FASD)
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Recent Advances in Fetal Alcohol Spectrum Disorder (FASD)

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Developmental Neuroscience".

Deadline for manuscript submissions: closed (15 December 2020) | Viewed by 37315

Special Issue Editor

Dr. Balapal S. Basavarajappa

E-Mail Website
Guest Editor
1. Department of Psychiatry, New York University Langone Medical Center, New York City, NY, USA
2. Scientist, Faculty at Columbia University Medical Center, Center for Dementia Research, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, NY, USA
Interests: endocannabinoids; synaptic plasticity; FASD; AUD; neurodegeneration; learning and memory; epigenetics; gene expression; behavior
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fetal alcohol spectrum disorder (FASD) is a disability in a child that results from alcohol exposure during the mother's pregnancy. FASD signs and symptoms may include any combination of physical defects, intellectual or cognitive disabilities, and difficulties functioning, interacting with others, and managing daily life. Alcohol exposure during pregnancy and its influence on offspring have been acknowledged for centuries, but only lately have we started to gain an understanding of the molecular mechanisms involved in FASD. The severity of FASD is influenced by the level of alcohol exposure, the developmental age, and the duration of the exposure (chronic vs. acute). In this regard, several studies in recent years have brought to light the critical role of different signaling receptors, epigenetic changes, and gene expression pathways in cognitive function. The aim of this Special Issue is to take stock of recent advancements and compare different molecular pathways and pharmacology strategies that can interact at both the cellular and behavioral levels.

We welcome both original basic or translation research papers and short communications presenting data that have a significant impact on our understanding of FASD. Also of interest are reviews that focus on molecular mechanisms involved in FASD or the impact of potential drugs that target behavioral outcomes.

Dr. Balapal S. Basavarajappa
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • FASD
  • Learning and Memory
  • Synaptic Plasticity
  • Alcohol

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Published Papers (2 papers)

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Research

20 pages, 2608 KiB  
Article
Prenatal Alcohol Exposure and the Facial Phenotype in Adolescents: A Study Based on Meconium Ethyl Glucuronide
by Janina Maschke, Jakob Roetner, Tamme W. Goecke, Peter A. Fasching, Matthias W. Beckmann, Oliver Kratz, Gunther H. Moll, Bernd Lenz, Johannes Kornhuber, Anna Eichler and IMAC-Mind-Consortium
Brain Sci. 2021, 11(2), 154; https://doi.org/10.3390/brainsci11020154 - 25 Jan 2021
Cited by 9 | Viewed by 32645
Abstract
Here, we explore the effects of prenatal alcohol exposure (PAE) in adolescence. We investigated associations between meconium ethyl glucoronide (EtG) and facial malformation. For 129 children (66/63 male/female; M = 13.3, SD = 0.32, 12–14 years), PAE was implemented by newborn meconium EtG [...] Read more.
Here, we explore the effects of prenatal alcohol exposure (PAE) in adolescence. We investigated associations between meconium ethyl glucoronide (EtG) and facial malformation. For 129 children (66/63 male/female; M = 13.3, SD = 0.32, 12–14 years), PAE was implemented by newborn meconium EtG and maternal self-reports during the third trimester. Cognitive development was operationalized by standardized scores (WISC V). The EtG cut-off values were set at ≥10 ng/g (n = 32, 24.8% EtG10+) and ≥112 ng/g (n = 20, 15.5% EtG112+). The craniofacial shape was measured using FAS Facial Photographic Analysis Software. EtG10+− and EtG112+-affected children exhibited a shorter palpebral fissure length (p = 0.031/p = 0.055). Lip circularity was smaller in EtG112+-affected children (p = 0.026). Maternal self-reports were not associated (p > 0.164). Lip circularity correlated with fluid reasoning (EtG10+ p = 0.031; EtG112+ p = 0.298) and working memory (EtG10+ p = 0.084; EtG112+ p = 0.144). The present study demonstrates visible effects of the facial phenotype in exposed adolescents. Facial malformation was associated with a child’s cognitive performance in the alcohol-exposed group. The EtG biomarker was a better predictor than maternal self-reports. Full article
(This article belongs to the Special Issue Recent Advances in Fetal Alcohol Spectrum Disorder (FASD))
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14 pages, 1813 KiB  
Article
Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice
by Shivakumar Subbanna and Balapal S. Basavarajappa
Brain Sci. 2020, 10(5), 271; https://doi.org/10.3390/brainsci10050271 - 1 May 2020
Cited by 7 | Viewed by 3547
Abstract
Alcohol consumption by pregnant women may produce neurological abnormalities that affect cognitive processes in children and are together defined as fetal alcohol spectrum disorders (FASDs). However, the molecular underpinnings are still poorly defined. In our earlier studies, we found that ethanol exposure of [...] Read more.
Alcohol consumption by pregnant women may produce neurological abnormalities that affect cognitive processes in children and are together defined as fetal alcohol spectrum disorders (FASDs). However, the molecular underpinnings are still poorly defined. In our earlier studies, we found that ethanol exposure of postnatal day 7 (P7) mice significantly induced widespread neurodegeneration mediated via endocannabinoids (eCBs)/cannabinoid receptor type 1 (CB1R). In the current study, we examined changes in the β-catenin protein levels that are involved in the regulation of neuronal function including neuronal death and survival. We found that moderate- and high-dose postnatal ethanol exposure (PEE) significantly reduced active-β-catenin (ABC) (non-phosphorylated form) protein levels in the hippocampus (HP) and neocortex (NC). In addition, we found that moderate- and high-dose PEE significantly increased the phosphorylated-β-catenin (p-β-catenin)/ABC ratios in the HP and NC. Antagonism/null mutation of CB1R before PEE to inhibit CC3 production mitigated the loss of ABC protein levels. Collectively, these findings demonstrated that the CB1R/β-catenin signaling mechanism causes neurodegeneration in neonatal mouse brains following PEE. Full article
(This article belongs to the Special Issue Recent Advances in Fetal Alcohol Spectrum Disorder (FASD))
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