Fetal alcohol syndrome: cardiac birth defects in mice and prevention with folate

Serrano, Maria; Han, Mingda; Brinez, Pilar; Linask, Kérsti K.

doi:10.1016/j.ajog.2010.03.017

Cited by 96 publications

(142 citation statements)

References 40 publications

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“…Several lines of animal research suggest the promise of various prenatal and neonatal interventions, including prenatal and postnatal treatment with neuroprotective Child Psychiatry Hum Dev peptides [127] and various nutrients [128][129][130][131][132]. Other research has demonstrated positive effects of neonatal handling, postnatal environment enrichment, and rehabilitative training on rats and mice with perinatal alcohol exposure [133].…”

Section: Treatmentmentioning

confidence: 99%

Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Proposed DSM-5 Diagnosis

Kable

O’Connor

Olson

et al. 2015

Child Psychiatry Hum Dev

107

101

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Over the past 40 years, a significant body of animal and human research has documented the teratogenic effects of prenatal alcohol exposure (PAE). Neurobehavioral Disorder associated with PAE is proposed as a new clarifying term, intended to encompass the neurodevelopmental and mental health symptoms associated with PAE. Defining this disorder is a necessary step to adequately characterize these symptoms and allow clinical assessment not possible using existing physically-based diagnostic schemes. Without appropriate diagnostic guidelines, affected individuals are frequently misdiagnosed and treated inappropriately (often to their considerable detriment) by mental health, educational, and criminal justice systems. Three core areas of deficits identified from the available research, including neurocognitive, self-regulation, and adaptive functioning impairments, are discussed and information regarding associated features and disorders, prevalence, course, familial patterns, differential diagnosis, and treatment of the proposed disorder are also provided.

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Section: Treatmentmentioning

confidence: 99%

Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Proposed DSM-5 Diagnosis

Kable

O’Connor

Olson

et al. 2015

Child Psychiatry Hum Dev

107

101

View full text Add to dashboard Cite

show abstract

“…A study using cell culture found that cell-cell adhesion was affected following the addition of ethanol to cells (Ramanathan et al, 1996). Furthermore, transcriptional changes have also been identified in various models of prenatal ethanol exposure affecting numerous signaling cascades critical for normal embryogenesis: the sonic hedgehog signaling cascade (Ahlgren et al, 2002;Li et al, 2007;Vangipuram and Lyman, 2012), the Wnt/β catenin signalling pathway (Serrano et al, 2010;Vangipuram and Lyman, 2012;Tong et al, 2013), and the Notch signalling pathway (Sathyan et al, 2007;Tong et al, 2013). Collectively, these studies indicate that alcohol is likely to act via a combination of mechanisms to induce fetal teratogenesis.…”

Section: Evidence In Animal Modelsmentioning

confidence: 93%

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Yamada¹

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The in utero environment is a critical determinant of the immediate and future health of the developing fetus. In Australia, two of the most commonly used drugs during pregnancy are alcohol and nicotine. Prolonged periods of gestational exposure to alcohol and nicotine, separately, have been associated with a range of adverse outcomes in the offspring, in both humans and experimental animal models. The consequences of ethanol and nicotine exposure restricted to early gestation on resultant offspring are poorly characterised, and few animal models exist to build greater understanding. Moreover, the immediate molecular changes associated with exposures to ethanol and/or nicotine restricted to early gestation has yet to be described.This thesis utilised mouse models of early gestational ethanol and/or nicotine exposure to explore the impact of each of these exposures on offspring growth, as well as their associated transcriptional and epigenetic changes. In each model, pregnant C57BL/6 dams were provided with ad libitum access to solutions of 10% ethanol and/or 100 µg/ml nicotine from fertilisation (0.5 dpc) to midgestation (8.5 dpc). The exposure window utilised in each of the models is developmentally equivalent to the first three to four weeks of a human pregnancy.Previously, our laboratory identified reduced growth, microcephaly, and gene expression changes in the liver and hippocampus of the postnatal offspring of the model of prenatal ethanol exposure utilised in this thesis. In contrast, at mid-gestation (9.5 dpc), there was no evidence of developmental delay (somite number), reduced growth (crown-rump length), or microcephaly.Further, a genome-wide gene expression microarray (targeting 30 855 genes) and a screen of the expression of 641 microRNAs, identified only one gene (Bcl11b) as differentially expressed in male 9.5 dpc whole embryos following the ethanol exposure. These data suggest that there is a delay between the ethanol exposure and the onset of adverse phenotypes -arguing that the embryo is somehow able to form a memory of the ethanol exposure. The absence of widespread transcriptional changes suggests that changes in embryonic mRNA and microRNA expression are unlikely to be major contributors to the memory of the exposure.A early gestational model of nicotine exposure was newly established in this thesis. This nicotine exposure resulted in an average serum cotinine (metabolite of nicotine) concentration similar to that reported in humans who smoke 10 to 15 cigarettes per day. This exposure was sufficient to induce a reduction in body size both at mid-gestation and postnatally, but not at late gestation. Furthermore, the increased expression of Zscan10 in the whole male 9.5 dpc embryo was identified and validated across multiple cohorts. Zscan10 encodes for a transcription factor expressed throughout development, with a proposed role in the regulation of progenitor cells. The increased expression of Zscan10 in the nicotine-exposed embryos was associated with a reduction in DNA methylation ...

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“…The few studies that have measured cardiac function in FASD animal models support the hypothesis that CHDs arising from ethanol exposure could have a significant contribution from abnormal function [26]. Abnormal embryonic cardiac function (as well as abnormal valves) was identified through ultrasound and histology, respectively at late stages (embryonic day 15.5) [italics researchers] of mouse development after ethanol exposure at gastrulation [27,28]. Functional and structural defects, including anomalies in heart volume/ morphology and conduction, were observed in latestage zebrafish after ethanol exposure, thus mimicking malformations occurring in patients with FASD [29].…”

Section: Congenital Heart Defects and Fetal Alcohol Spectrum Disordermentioning

confidence: 99%

Fetal Alcohol Spectrum Disorder: Risk for Diabetes and Congenital Heart Defects

Salmon

2018

IDCD

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Excessive use of alcohol can be a cause for many disease and injury conditions. These include amongst many others, myocardial infarction, diabetes mellitus, atrial fibrillation, nonischaemic cardiomyopathy, fetal alcohol spectrum disorder (FASD), congenital heart defects (CHD) and liver cirrhosis. Even low levels of prenatal alcohol (ethanol) exposure, such as in a single dose, can produce birth defects termed fetal alcohol syndrome (FAS) which is the highest marker on the spectrum. Diabetes is regarded as a major cause of cardiovascular disease whilst prenatal alcohol exposure (PAE) can range from no observable adverse effects to mortality. CHD are stated to be the most prevalent cause of mortality in individuals with FASD. The dimension of the problems is still greatest in the Western world although it is stated to be the leading cause of mental retardation in North America.FASD is a neurodevelopmental disability which can be occasioned when a pregnant woman consumes alcohol. The diagnostic criteria for FASD includes growth impairment, abnormal facial features and neurocognitive impairments. The most frequently reported abnormal facial features in FASD are thin upper lip, indistinct or smooth philtrum and short palpebral fissure length. Other features are microganthia, low set ears, ptosis, absent or indistinct philtral ridge, epicanthal folds, cleft palate, flat nasal bridge and midface hypoplasia. The neurocognitive features commonly reported in FASD are microcephaly, intellectual disability, attention-deficit hyperactivity disorder (ADHD) and behavioural impairments. Central nervous system (CNS) injury is also seen and is debilitating. Structural abnormalities of the CNS can include microcephaly, agenesis/absence of the corpus callosum and multiple severe brain malformations. This review article seeks to address the association of FASD with diabetes and CHD.

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Fetal alcohol syndrome: cardiac birth defects in mice and prevention with folate

Cited by 96 publications

References 40 publications

Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Proposed DSM-5 Diagnosis

Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Proposed DSM-5 Diagnosis

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Fetal Alcohol Spectrum Disorder: Risk for Diabetes and Congenital Heart Defects

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