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National Organization on Fetal Alcohol Syndrome, Protecting children and families by fighting the leading known cause of mental retardation and birth defects
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“I've learned to cope with my disability. I've come to terms with the fact that I have fetal alcohol syndrome. I had spent my whole life feeling sorry for myself, going 'why did this happen to me' and blaming my mother for it, because she drank. But blaming others for it wasn't going to make it easy. Now I'm actually in a position where I can help others with their disabilities because I can relate to them.”
Erica Gites-Miles

Health Care Professionals

Weekly Research Spotlight

Compiled by Michael Ybarra

Prevention of alcohol-induced developmental delays and learning abnormalities in a model of fetal alcohol syndrome

Researchers at the National Institute of Child Health and Human Development have found a way to minimize the deleterious affects of prenatal alcohol exposure on developmental and learning abnormalities in a model of fetal alcohol syndrome.  The objective of their work, published recently in the American Journal of Obstetrics and Gynecology, was to evaluate whether activity-dependent neurotrophic factor-12 could prevent alcohol-induced damage in a well-studied mouse model.  The mice were given alcohol plus activity-dependent neurotrophic factor-12 on day 8 of gestation and their offspring were compared to those of mothers given alcohol alone.  Fetal death was decreased when mothers were pretreated with activity-dependent neurotrophic factor-12.  Developmental milestones were also measured, and the pretreated mother’s gave birth to offspring that were no different from placebo, and significantly better than alcohol alone at mastering a Morris water maze and a hole punch activity.  The researchers concluded that “activity-dependent neurotrophic factor-12 prevents alcohol-induced fetal death and developmental learning abnormalities in a model of FAS.”

Mitochondrially targeted vitamin E and vitamin E mitigate ethanol-mediated effects on cerebellar granule cell antioxidant defense system

Animal studies have revealed that prenatal exposure to alcohol can cause mitochondrial dysfunction, intracellular oxidant accumulation, and suppression of endogenous antioxidants defense systems.  Marieta Heaton’s group at the McKnight Brain Institute of the University of Florida is actively researching the cellular mechanisms that underlie alcohol-induced damage and the protective mechanisms of potential therapeutics against prenatal alcohol exposure.  Previous studies from this group show that, in vivo, natural vitamin E reduces neuronal death in the cerebellum of alcohol-exposed animals.  In vitro studies show that natural vitamin E prevents apoptosis and necrosis in alcohol-exposed cerebellar granule cells.  The most recent study by Kendra Siler-Marsiglio et al., shows that vitamin E chemically-engineered to target the mitochondria inhibits intracellular oxidant accumulation, mitigates alcohol-mediated suppression of antioxidant systems, and promotes cell survival at much lower concentrations than natural vitamin E. This modified vitamin E, targets the mitochondria and provides significant neuroprotection against alcohol concentrations as high as 1600 mg/dl. Bioavailability studies of orally-administered mitochondrially-targeted vitamin E show that it can cross the blood-placenta barrier of pregnant dams to reach the fetus and the blood-brain barrier; both are essential for a FAS therapy. Mitochondrially-targeted vitamin E shows promise as a future therapeutic strategy against damage and death cause by prenatal alcohol exposure. Brain Res. 2005 Jul 15; [Epub ahead of print]

Alcohol Inhibits Survival Signals in the Cerebellum of an FAS Animal Model

Alcohol inhibits insulin-stimulated survival signals causing cerebellar hypoplasia in the developing brain, according to researchers at the Rhode Island Hospital.  Using a rat model of FAS, this study found a decreased expression of the insulin gene in the cerebella of exposed rats.  Alcohol exposure also caused a decrease in the amount of insulin, insulin-like growth factor receptor tyrosine kinase, glucose transport molecules, and steady-state levels of ATP in the cells of the cerebellum.  These results suggest cerebellar hypoplasia resulting from prenatal alcohol exposure is caused by a deficient energy supply.  Cell Mol Life Sci. 2005 May;62(10):1131-45.

Prenatal Alcohol Exposure Alters Maternal and Fetal Endocrine Systems

Studies done at the University of British Columbia may have uncovered the link between prenatal alcohol exposure and some of the long-term symptoms of FASD.  Alcohol consumption affects both the maternal and fetal endocrine systems, altering the interaction between maternal-fetal hormones.  Additionally, exposure to alcohol can cause reprogramming of the hypothalamic-pituitary-adrenal (HPA) axis in the fetus so that HPA tone is increased throughout life.  Increasing HPA tone causes excess secretion of glucocorticoids.  This in turn leads to altered behavioral and physiologic responses.  Glucocorticoid secretion also causes suppression of the immune system which will increase the individual’s vulnerability to disease later in life.  The endocrine affects of alcohol exposure may explain the behavioral, cognitive, and immune deficits seen in patients with FASD.  Exp Biol Med (Maywood). 2005 Jun;230(6):376-88.

Ercc61 May Play a Role in the Tertogenic Action of Alcohol

Researchers at Peking University’s School of Public Health have discovered a mouse gene, Ercc61 that may account for the mutagenic affects of prenatal alcohol exposure.  Ercc61 is normally expressed in the neural tube and heart of a 10.5-day old mouse embryo.  Expression of Ercc61 was significantly down-regulated after in-utero alcohol exposure on days 6-10.  On day 15, expression of Ercc61 in the brain and heart (the two organs most affected by Fetal Alcohol Syndrome), were markedly decreased following alcohol exposure.  This result suggests Ercc61 might play a role in the mutagenic affects of alcohol consumption during pregnancy.  Toxicol Let. 2005 Jul 4;157(3):233-9

Research Investigating Effects of Alcohol and Developing Brain Cells
Even brief exposures to small amounts of alcohol may kill brain cells in a developing fetus. A study carried out by John Olney, M.D., at the Washington School of Medicine in St. Louis showed that just two drinks consumed during pregnancy may be enough to kill some developing brain cells, leading to permanent brain damage. Nerve cells will die if they fail to make synaptic connections in time. Drinking alcohol can interfere with the formation of these connections. Based on the animal studies carried out by Dr. Olney, it does not take much alcohol to have this effect. In unborn mice, the concentration of alcohol needed to kill developing brain cells was 0.07 percent. In most women, two cocktails is enough to elevate blood alcohol levels to this amount. Dr. Olney's advice is for pregnant women to completely avoid alcohol until further research can better explain the sensitivity of developing brain cells to alcohol.
Addiction Biology 2004 Jun;9(2):137-49

Nerve Damage Caused by Prenatal Alcohol Exposure
It is well known that prenatal alcohol exposure can cause damage to the central nervous system. But a study conducted by the National Institute of Child Health and Human Development at the National Institutes of Health showed that babies can suffer nerve damage in the arms and legs, too. Researchers compared 17 full-term newborns whose mothers drank heavily while pregnant with 13 newborns whose mothers did not drink. "Heavy drinking" was defined as having four or more standard drinks a day—a standard drink being a can of beer, one glass of wine or one mixed drink.

Babies exposed to alcohol showed nerve damage in their arms and legs at both one month and one year of age, suggesting developing nerve cells were permanently damaged. The researchers will continue to study these children to find out the long-term effects of alcohol exposure on nerve function, motor skills and touch sensation.


From the CDC: New! FAS Guidelines for Referral and Diagnosis

NIH News: New Study Finds Babies Born To Mothers Who Drink Alcohol Heavily May Suffer Permanent Nerve Damage

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