Disease relevance of Fetal Alcohol Syndrome

• The fact that PACAP prevented ethanol toxicity even when added 2 h after alcohol exposure, suggests that selective PACAP agonists could have potential therapeutic value for the treatment of fetal alcohol syndrome [1].
• The observation that blocking Sonic hedgehog (Shh) signaling results in similar craniofacial abnormalities prompted us to examine whether there was a link between this aspect of fetal alcohol syndrome and loss of Shh [2].
• Ethanol (EtOH) disrupts the structure and function of the developing nervous system, sometimes leading to birth defects associated with fetal alcohol syndrome (FAS) [3].
• Ethanol-associated selective fetal malnutrition: a contributing factor in the fetal alcohol syndrome [4].
• Maternal consumption of ethanol produces a pattern of malformations, including nervous system abnormalities, in the developing fetus, a state called Fetal Alcohol Syndrome [5].

Psychiatry related information on Fetal Alcohol Syndrome

• In conclusion, by altering VTA neuronal function, ethanol-induced changes in glycine receptors may contribute to neurobehavioral manifestations of the fetal alcohol syndrome [6].
• Although neonatal withdrawal syndrome is often noted in infants of narcotics addicts, ethanol withdrawal has been reported only among neonates with fetal alcohol syndrome [7].
• Fetal alcohol syndrome (FAS) is characterized by growth retardation, mental deficiencies, and numerous craniofacial and neuronal anomalies; the type and severity of these defects may be related to the time and dose of maternal ethanol exposure [8].
• Chronic exposure to elevated glutamate during critical periods of brain development may contribute to the pathogenesis of the fetal alcohol syndrome [9].
• Children of women who abuse alcohol during pregnancy may be affected by varying degrees of neurological abnormality, even if they are not diagnosed with Fetal Alcohol Syndrome [10].

High impact information on Fetal Alcohol Syndrome

• Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome [11].
• Acetaldehyde and the fetal alcohol syndrome [12].
• Metronidazole and the fetal alcohol syndrome [13].
• Also addressed are retinoid-androgen interactions and evidence incompatible with ethanol causing fetal alcohol syndrome by competing directly with retinol dehydrogenation to impair retinoic acid biosynthesis [14].
• Ethanol's inhibition of the NMDA receptor in the fetal brain likely contributes to the CNS manifestations of fetal alcohol syndrome [15].

Chemical compound and disease context of Fetal Alcohol Syndrome

• Twenty subjects with confirmed prenatal alcohol exposure (10 of whom were diagnosed as having Fetal Alcohol Syndrome) and 20 normal controls matched for age, gender, and ethnic background participated [16].
• Data from the patients herein described and the available scientific literature suggest that the mechanism of alcohol craniofacial teratogenesis may be nonspecific, with a variety of teratogens, including toluene, giving rise to phenotypic facial abnormalities similar to those of the fetal alcohol syndrome [17].
• Ethanol triggers massive apoptotic neurodegeneration in the developing brain by interfering with both the NMDA and GABA(subscript)A(/subscript) receptor systems, and this can explain the reduced brain mass and lifelong neurobehavioral disturbances associated with intrauterine exposure of the human fetus to ethanol (fetal alcohol syndrome) [18].
• We conclude that patients with fetal alcohol syndrome have a defect in distal acidification and potassium excretion which cannot be attributed to abnormal aldosterone secretion [19].
• Inhibition of retinoic acid synthesis and its implications in fetal alcohol syndrome (FAS) [20].

Biological context of Fetal Alcohol Syndrome

• Epidemiology of fetal alcohol syndrome in a South African community in the Western Cape Province [21].
• In utero ethanol suppresses cerebellar activator protein-1 and nuclear factor-kappa B transcriptional activation in a rat fetal alcohol syndrome model [22].
• Ethanol effects on embryonic craniofacial growth and development: implications for study of the fetal alcohol syndrome [23].
• The incidence of Fetal Alcohol Syndrome is now estimated at 0.97 cases per 1,000 live births in the general obstetric population and 4.3% among "heavy" drinkers [24].
• CONCLUSIONS: These results suggest that ethanol-induced death of insulin-stimulated immature neuronal cells is mediated in part by impaired Mt function associated with Mt DNA damage and reduced Mt mass, and therefore it is likely to contribute to neuronal loss associated with fetal alcohol syndrome [25].

Anatomical context of Fetal Alcohol Syndrome

• The potential interference of retinol metabolism by ethanol through the ADH pathway may play a significant role in the pathogenesis of fetal alcohol syndrome and alcohol-related upper digestive tract cancer [26].
• It is also suggested that L1 is a direct target of ethanol in fetal alcohol syndrome, since ethanol inhibits the aggregation of cultured cells expressing L1 (Ramanathan, R., Wilkemeyer, M. F., Mittel, B., Perides, G., and Charness, M. E. (1996) J. Cell Biol. 133, 381-390) [27].
• Alteration of the phospholipid profile in the hippocampus resulting from exposure to ethanol during prenatal and developmental stages may have significant implications with respect to the cognitive dysfunction observed in fetal alcohol syndrome [28].
• To investigate the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in fetal alcohol syndrome (FAS)-associated ocular injury, two antioxidant enzymes, catalase and peroxiredoxin 5, were overexpressed in the two blastomeres of the two-cell stage Xenopus embryos [29].
• BACKGROUND: Ethanol inhibition of insulin signaling pathways may contribute to impaired central nervous system (CNS) development in the fetal alcohol syndrome and brain atrophy associated with alcoholic neurodegeneration [30].

Gene context of Fetal Alcohol Syndrome

• In addition, the finding of endogenous RA and class IV ADH mRNA in the craniofacial region has implications for the mechanism of fetal alcohol syndrome [31].
• N-methyl-D-aspartate receptor dysfunction has been strongly suggested to link with the abnormalities seen in fetal alcohol syndrome [32].
• Differential expression of c-fos in a mouse model of fetal alcohol syndrome [33].
• Thus, embryonic ADH can presumably be induced by retinoic acid, further strengthening the argument that ADH plays a role in embryonic retinoic acid synthesis and fetal alcohol syndrome [34].
• This alteration in NMDA receptor subunits may underlie the learning abnormalities in fetal alcohol syndrome [35].

Analytical, diagnostic and therapeutic context of Fetal Alcohol Syndrome

• clinical observation and experimental animal models indicate that chronic ethanol ingestion during pregnancy results in a well recognized state in the fetus termed fetal alcohol syndrome [36].
• The principal features of fetal alcohol syndrome (FAS) include microcephaly, reduced body size, and characteristic facial malformation, most of which are associated with hypoplasticity of structures around the mouth [37].
• This required a complete evaluation to discard other conditions that present with low psychomotor development and distinctive facies, such as Kabuki syndrome or fetal alcohol syndrome [38].

References