The Effects of Timing and Duration of Alcohol Exposure on Development of the Fetal Brain

2022 ◽  
pp. 27-50
Author(s):  
Susan E. Maier ◽  
Wei-Jung A. Chen ◽  
James R. West
Keyword(s):  
Fetal Brain ◽  
Alcohol Exposure

scholarly journals An enriched biosignature of gut microbiota-dependent metabolites characterizes maternal plasma in a mouse model of fetal alcohol spectrum disorder

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Manjot S. Virdee ◽  
Nipun Saini ◽  
Colin D. Kay ◽  
Andrew P. Neilson ◽  
Sze Ting Cecilia Kwan ◽  
...  
Keyword(s):  
Phenolic Acids ◽  
Fetal Liver ◽  
Prenatal Alcohol Exposure ◽  
Fetal Brain ◽  
Principal Component ◽  
Alcohol Exposure ◽  
Maternal Plasma ◽  
Cognitive Disability ◽  
Fetal Alcohol ◽  
Network Analyses

AbstractPrenatal alcohol exposure (PAE) causes permanent cognitive disability. The enteric microbiome generates microbial-dependent products (MDPs) that may contribute to disorders including autism, depression, and anxiety; it is unknown whether similar alterations occur in PAE. Using a mouse PAE model, we performed untargeted metabolome analyses upon the maternal–fetal dyad at gestational day 17.5. Hierarchical clustering by principal component analysis and Pearson’s correlation of maternal plasma (813 metabolites) both identified MDPs as significant predictors for PAE. The majority were phenolic acids enriched in PAE. Correlational network analyses revealed that alcohol altered plasma MDP-metabolite relationships, and alcohol-exposed maternal plasma was characterized by a subnetwork dominated by phenolic acids. Twenty-nine MDPs were detected in fetal liver and sixteen in fetal brain, where their impact is unknown. Several of these, including 4-ethylphenylsulfate, oxindole, indolepropionate, p-cresol sulfate, catechol sulfate, and salicylate, are implicated in other neurological disorders. We conclude that MDPs constitute a characteristic biosignature that distinguishes PAE. These MDPs are abundant in human plasma, where they influence physiology and disease. Their altered abundance here may reflect alcohol’s known effects on microbiota composition and gut permeability. We propose that the maternal microbiome and its MDPs are a previously unrecognized influence upon the pathologies that typify PAE.

scholarly journals Thiamin deficiency on fetal brain development with and without prenatal alcohol exposure

2018 ◽  
Vol 96 (2) ◽  
pp. 169-177 ◽  
Author(s):  
Olena Kloss ◽  
N.A. Michael Eskin ◽  
Miyoung Suh
Keyword(s):  
Brain Development ◽  
Prenatal Exposure ◽  
Prenatal Alcohol Exposure ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Brain Dysfunction ◽  
Negative Effects ◽  
Thiamin Deficiency ◽  
Optimal Health ◽  
Fetal Brain Development

Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, γ-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD.

scholarly journals Fetal alcohol exposure reduces responsiveness of taste nerves and trigeminal chemosensory neurons to ethanol and its flavor components

2017 ◽  
Vol 118 (2) ◽  
pp. 1198-1209 ◽  
Author(s):  
John I. Glendinning ◽  
Joyce Tang ◽  
Ana Paula Morales Allende ◽  
Bruce P. Bryant ◽  
Lisa Youngentob ◽  
...  
Keyword(s):  
Fetal Brain ◽  
Alcohol Exposure ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
Chemosensory Neurons ◽  
Adolescent Alcohol ◽  
Flavor Components ◽  
Fetal Brain Development ◽  
Adolescent Rats ◽  
Pregnant Mothers

Pregnant mothers are advised to avoid alcohol. This is because even small amounts of alcohol can alter fetal brain development and increase the risk of adolescent alcohol abuse. We asked how fetal alcohol exposure (FAE) produces the latter effect in adolescent rats by measuring responsiveness of taste nerves and trigeminal chemosensory neurons. We found that FAE substantially reduced taste and trigeminal responsiveness to ethanol and its flavor components.

scholarly journals VP24.11: Prenatal alcohol exposure affects specific fetal brain structures: an atlas‐based fetal MRI study

2021 ◽  
Vol 58 (S1) ◽  
pp. 203-203
Author(s):  
M. Stuempflen ◽  
E. Schwartz ◽  
M.C. Diogo ◽  
S. Glatter ◽  
B. Pfeiler ◽  
...  
Keyword(s):  
Prenatal Alcohol Exposure ◽  
Fetal Brain ◽  
Fetal Mri ◽  
Alcohol Exposure ◽  
Brain Structures ◽  
Prenatal Alcohol ◽  
Mri Study

scholarly journals Alcohol exposure during late gestation: multiple developmental outcomes in sheep

2012 ◽  
Vol 3 (4) ◽  
pp. 224-236 ◽  
Author(s):  
K. Kenna ◽  
F. Sozo ◽  
R. De Matteo ◽  
T. Hanita ◽  
S. P. Gray ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Mrna Expression ◽  
Phospholipid Composition ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Left Ventricular ◽  
Late Gestation ◽  
Fetal Alcohol Exposure ◽  
Fetal Alcohol ◽  
Wall Stiffness

Alcohol consumption during pregnancy remains common in many countries. Exposure to even low amounts of alcohol (i.e. ethanol) in pregnancy can lead to the heterogeneous fetal alcohol spectrum disorders (FASD), while heavy alcohol consumption can result in the fetal alcohol syndrome (FAS). FAS is characterized by cerebral dysfunction, growth restriction and craniofacial malformations. However, the effects of lower doses of alcohol during pregnancy, such as those that lead to FASD, are less well understood. In this article, we discuss the findings of recent studies performed in our laboratories on the effects of fetal alcohol exposure using sheep, in which we investigated the effects of late gestational alcohol exposure on the developing brain, arteries, kidneys, heart and lungs. Our studies indicate that alcohol exposure in late gestation can (1) affect cerebral white matter development and increase the risk of hemorrhage in the fetal brain, (2) cause left ventricular hypertrophy with evidence of altered cardiomyocyte maturation, (3) lead to a decrease in nephron number in the kidney, (4) cause altered arterial wall stiffness and endothelial and smooth muscle function and (5) result in altered surfactant protein mRNA expression, surfactant phospholipid composition and pro-inflammatory cytokine mRNA expression in the lung. These findings suggest that fetal alcohol exposure in late gestation can affect multiple organs, potentially increasing the risk of disease and organ dysfunction in later life.

Effect of alcohol exposure on fetal brain development

2013 ◽  
Author(s):  
Narendran Sudheendran ◽  
Shameena Bake ◽  
Rajesh C. Miranda ◽  
Kirill V. Larin
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Fetal Brain Development
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