Difference between revisions of "Talk:Abnormal Development - Fetal Alcohol Syndrome"

From Embryology
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"More episodes of this treatment were for alcohol than any other drug type, and this proportion has now risen four years in a row. ...As seen in previous years, most treatment episodes (66%) were provided to male clients."
 
"More episodes of this treatment were for alcohol than any other drug type, and this proportion has now risen four years in a row. ...As seen in previous years, most treatment episodes (66%) were provided to male clients."
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===Prenatal alcohol exposure triggers ceramide-induced apoptosis in neural crest-derived tissues concurrent with defective cranial development===
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Cell Death Dis. 2010 May 27;1(5):e46.
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Wang G, Bieberich E.
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Source
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Institute of Molecular Medicine and Genetics, School of Medicine, Medical College of Georgia, Augusta, GA 30912, USA.
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Abstract
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Fetal alcohol syndrome (FAS) is caused by maternal alcohol consumption during pregnancy. The reason why specific embryonic tissues are sensitive toward ethanol is not understood. We found that in neural crest-derived cell (NCC) cultures from the first branchial arch of E10 mouse embryos, incubation with ethanol increases the number of apoptotic cells by fivefold. Apoptotic cells stain intensely for ceramide, suggesting that ceramide-induced apoptosis mediates ethanol damage to NCCs. Apoptosis is reduced by incubation with CDP-choline (citicoline), a precursor for the conversion of ceramide to sphingomyelin. Consistent with NCC cultures, ethanol intubation of pregnant mice results in ceramide elevation and increased apoptosis of NCCs in vivo. Ethanol also increases the protein level of prostate apoptosis response 4 (PAR-4), a sensitizer to ceramide-induced apoptosis. Prenatal ethanol exposure is concurrent with malformation of parietal bones in 20% of embryos at day E18. Meninges, a tissue complex derived from NCCs, is disrupted and generates reduced levels of TGF-β1, a growth factor critical for bone and brain development. Ethanol-induced apoptosis of NCCs leading to defects in the meninges may explain the simultaneous presence of cranial bone malformation and cognitive retardation in FAS. In addition, our data suggest that treatment with CDP-choline may alleviate the tissue damage caused by alcohol.
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PMID: 21364652
  
 
==2009==
 
==2009==

Revision as of 09:41, 22 April 2011

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Cite this page: Hill, M.A. (2020, March 30) Embryology Abnormal Development - Fetal Alcohol Syndrome. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Fetal_Alcohol_Syndrome

2011

Fetal Alcohol Spectrum Disorders: An Overview

Neuropsychol Rev. 2011 Apr 16. [Epub ahead of print]

Riley EP, Infante MA, Warren KR. Source Department of Psychology, Center for Behavioral Teratology, San Diego State University, 6330 Alvarado Court, Suite 100, San Diego, CA, 92120, USA, eriley@mail.sdsu.edu.

Abstract

When fetal alcohol syndrome (FAS) was initially described, diagnosis was based upon physical parameters including facial anomalies and growth retardation, with evidence of developmental delay or mental deficiency. Forty years of research has shown that FAS lies towards the extreme end of what are now termed fetal alcohol spectrum disorders (FASD). The most profound effects of prenatal alcohol exposure are on the developing brain and the cognitive and behavioral effects that ensue. Alcohol exposure affects brain development via numerous pathways at all stages from neurogenesis to myelination. For example, the same processes that give rise to the facial characteristics of FAS also cause abnormal brain development. Behaviors as diverse as executive functioning to motor control are affected. This special issue of Neuropsychology Review addresses these changes in brain and behavior highlighting the relationship between the two. A diagnostic goal is to recognize FAS as a disorder of brain rather than one of physical characteristics.

PMID: 21499711

2010

Alcohol and other drug treatment services in Australia 2006–07

Around 143,000 alcohol and other drug treatment episodes were provided in Australia in 2008-09'

Australian Institute of Health and Welfare 2008. Alcohol and other drug treatment services in Australia 2006–07: report on the National Minimum Data Set. Drug treatment series no. 8. Cat. no. HSE 59. Canberra: AIHW.

"More episodes of this treatment were for alcohol than any other drug type, and this proportion has now risen four years in a row. ...As seen in previous years, most treatment episodes (66%) were provided to male clients."

Prenatal alcohol exposure triggers ceramide-induced apoptosis in neural crest-derived tissues concurrent with defective cranial development

Cell Death Dis. 2010 May 27;1(5):e46.

Wang G, Bieberich E. Source Institute of Molecular Medicine and Genetics, School of Medicine, Medical College of Georgia, Augusta, GA 30912, USA.

Abstract

Fetal alcohol syndrome (FAS) is caused by maternal alcohol consumption during pregnancy. The reason why specific embryonic tissues are sensitive toward ethanol is not understood. We found that in neural crest-derived cell (NCC) cultures from the first branchial arch of E10 mouse embryos, incubation with ethanol increases the number of apoptotic cells by fivefold. Apoptotic cells stain intensely for ceramide, suggesting that ceramide-induced apoptosis mediates ethanol damage to NCCs. Apoptosis is reduced by incubation with CDP-choline (citicoline), a precursor for the conversion of ceramide to sphingomyelin. Consistent with NCC cultures, ethanol intubation of pregnant mice results in ceramide elevation and increased apoptosis of NCCs in vivo. Ethanol also increases the protein level of prostate apoptosis response 4 (PAR-4), a sensitizer to ceramide-induced apoptosis. Prenatal ethanol exposure is concurrent with malformation of parietal bones in 20% of embryos at day E18. Meninges, a tissue complex derived from NCCs, is disrupted and generates reduced levels of TGF-β1, a growth factor critical for bone and brain development. Ethanol-induced apoptosis of NCCs leading to defects in the meninges may explain the simultaneous presence of cranial bone malformation and cognitive retardation in FAS. In addition, our data suggest that treatment with CDP-choline may alleviate the tissue damage caused by alcohol.

PMID: 21364652

2009

Magnetic resonance microscopy defines ethanol-induced brain abnormalities in prenatal mice: effects of acute insult on gestational day 8

Alcohol Clin Exp Res. 2009 Jun;33(6):1001-11. Epub 2009 Mar 19.


Parnell SE, O'Leary-Moore SK, Godin EA, Dehart DB, Johnson BW, Allan Johnson G, Styner MA, Sulik KK.

The Bowles Center for Alcohol Studies, and Neurodevelopmental Disorders Research Center, University of North Carolina, Chapel Hill, NC 27599-7178, USA. sparnell@med.unc.edu

http://www.ncbi.nlm.nih.gov/pubmed/19302087 http://www3.interscience.wiley.com/journal/122268272/abstract