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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol is a teratogen and it can cause lasting birth defects called Fetal Alcohol Syndrome (FAS)/Fetal Alcohol Effects (FAE). FAS is one of the leading causes of mental retardation. FAS/FAE can result in a myriad of behavioral, learning and developmental problems. There are estimates of 12,000 new cases of FAS yearly. The school nurse plays an important advocacy and educational role in helping the child with FAS. Family involvement is important for the child with FAS.
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PMID:FAS/FAE: impact on children. 1088 55

Prenatal exposure to alcohol is one of the leading preventable causes of birth defects, mental retardation, and neurodevelopmental disorders. In 1973, a cluster of birth defects resulting from prenatal alcohol exposure was recognized as a clinical entity called fetal alcohol syndrome. More recently, alcohol exposure in utero has been linked to a variety of other neurodevelopmental problems, and the terms alcohol-related neurodevelopmental disorder and alcohol-related birth defects have been proposed to identify infants so affected. This statement is an update of a previous statement by the American Academy of Pediatrics and reflects the current thinking about alcohol exposure in utero and the revised nosology.
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PMID:American Academy of Pediatrics. Committee on Substance Abuse and Committee on Children With Disabilities. Fetal alcohol syndrome and alcohol-related neurodevelopmental disorders. 1092 Jan 68

Pregnant rats were fed an ethanol-containing liquid diet between gestational day (GD) 10 and GD 21. Leptomeningeal heterotopias were observed in the cerebral cortex of ethanol-exposed fetuses. They appeared on the brain surface of the lateral cortical region near the rhinal fissure, and were found more numerously in the rostral than the caudal region. These abnormalities contained certain neuronal perikarya, microtubule-associated protein (MAP) 1b-positive neuronal processes, and Rat-401-positive radial glial fibers. Immunostaining for Rat-401 revealed that the heterotopias protruded through breaches in the glia limitans. In adult rats exposed to ethanol prenatally, the heterotopias persisted in the lateral cortical region. We conclude that prenatal exposure to ethanol might induce defects in the glia limitans, resulting in the genesis of leptomeningeal heterotopias. These abnormalities may be related to mental retardation or the cognitive deficits associated with human fetal alcohol syndrome (FAS).
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PMID:Prenatal exposure to ethanol induces leptomeningeal heterotopia in the cerebral cortex of the rat fetus. 1119 37

Fetal alcohol syndrome (FAS) is a collection of signs and symptoms seen in some children exposed to alcohol in the prenatal period. It is characterized mainly by physical and mental retardation, craniofacial anomalies and minor joint abnormalities. However, with the increasing incidence of FAS, there is a great variation in the clinical features of FAS. This article describes in detail these clinical features. Due to ethical reasons it is not possible to perform experiments on pregnant women. Hence to study the effects of alcohol, various animal and avian experimental models have been chosen. The various experimental findings and human correlation are described. The exact mechanism by which alcohol induces its teratogenic effects is not known. The possible mechanisms are discussed. Measures to prevent the occurrence of FAS have been suggested.
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PMID:Alcohol and the developing fetus--a review. 1120 51

Foetal alcohol syndrome is a syndrome with a rather high incidence. It is characterized by mental retardation, growth deficiency, a striking facial appearance (a.o. short palpebral fissures, short, upturned nose, hypoplastic philtrum, hypoplastic maxilla). Malocclusion and a disturbed facial growth may occur. Mental retardation can interfere with dental treatment.
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PMID:[Syndromes 19. Fetal alcohol syndrome]. 1138 71

Glial cells and their interactions with neurons play vital roles during the ontogeny of the nervous system and in the adult brain. Alcohol intake during pregnancy can cause mental retardation and neurobehavioral disorders as well as fetal alcohol syndrome (FAS). Clinical and experimental evidence indicate that in utero alcohol exposure induces structural and functional abnormalities in gliogenesis and in glial-neuronal interactions, suggesting a potential role of glial cells on ethanol-induced developmental brain abnormalities. In vivo studies have shown ethanol-associated alterations in the migration of neurons and radial glial as well as in astrogliogenesis and myelin development. In astrocytes in primary culture, ethanol has been found to (1) impair cell growth and differentiation, (2) decrease the levels of glialfibrillary acidic protein or GFAP (an astrocyte marker) and its gene expression and (3) interfere with the stimulatory effect of trophic factors affecting their release and receptor expression. Evidence also suggests that ethanol affects intracellular protein trafficking, which may mediate some effects of ethanol on astroglial cells. These findings suggest that glial cells are target of ethanol toxicity during brain development and may underlie the neurodevelopmental abnormalities observed after in utero alcohol exposure and in FAS.
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PMID:Glia and fetal alcohol syndrome. 1177 Aug 80

A major mechanism guiding neural development is through cell-cell and cell-matrix adhesions and signaling mediated by cell adhesion molecules (CAMs). The majority of CAMs have been grouped into three families: the cadherins, the integrins and the members of the immunoglobulin superfamily including L1. While the elucidation of new receptors and matrix components has become a frequent occurrence, the elucidation of the mechanisms by which they operate, and the function of those mechanisms in complex developmental events remains rudimentary. Members of all three families participate in differential adhesion, signal transduction and physical/mechanical effects. Each of these modes of action is a potential target for developmental neurotoxicants. In this brief review, the role of L1 in normal and abnormal neurodevelopment will be summarized. L1 is a cell surface transmembrane glycoprotein with a single copy gene on the X chromosome. There are two alternatively spliced exons, with the RSLE containing form found only on axons and growth cones of post-mitotic neurons. L1 mediates the following functions: adhesion, neurite extension, neuronal migration, and axon fasciculation. L1 is critical for normal neural development; humans with genetic defects in L1, termed corpus callosum hypoplasia, mental retardation, adducted thumbs, spasticity and hydrocephalus (CRASH) syndrome, and mice lacking expression of L1 have extensive neuropathologic and aberrant behaviors. The observation that patients with fetal alcohol syndrome share similar features to patients with CRASH has lead to the investigation of the effects of ethanol on L1. Physiologic concentrations of ethanol have been shown to inhibit L1 mediated neurite outgrowth in cerebellar granule neurons. Such inhibition may result from decreased expression, altered cell surface distribution, impaired signal transduction, or impaired interaction with the cytoskeleton. These data indicate that L1 and its associated signaling pathways are potentially targets for developmental neurotoxicants.
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PMID:L1 cell adhesion molecule signal cascades: targets for ethanol developmental neurotoxicity. 1177 Aug 84

Fetal alcohol syndrome (FAS) is the leading cause of mental retardation in western society. We investigated possible changes in glutamate receptor levels in neonatal animals following ethanol exposure using radioligand binding and western blot analysis. We used a vapor chamber to administer ethanol to neonatal Wistar rats 3 h a day from postnatal day (PND) 4-9. A separation control group was separated from their mothers for the same time and duration as the vapor treatment, while a normal control group was left to develop normally. Daily ethanol administrations resulted in decreased brain weight and body weight, as well as microencephaly (decreased brain:body weight ratio). Neither the affinity nor maximum binding of [(3)H]MK-801 (dizoclipine maleate) in the cortex of PND10 rats differed between treatment groups. Western blot analysis also failed to reveal any changes in NMDAR1, NMDAR2A, or NMDAR2B receptor levels. In contrast, the AMPA receptor subunit GluR1 was greatly reduced in vapor-treated pups compared with control pups, as revealed by western blot analysis. A similar reduction was found in westerns with an antibody recognizing the GluR2 and 4 subunits. These results indicate that ethanol reduces AMPA rather than NMDA receptors in the developing neocortex, possibly by blocking NMDA receptors during development.
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PMID:Neonatal ethanol exposure reduces AMPA but not NMDA receptor levels in the rat neocortex. 1203 20

Developmental neurotoxicity can be ascribed to in utero exposure to exogenous substances or to exposure of the fetus to endogenous compounds that accumulate because of genetic mutations. One of the best recognized human neuroteratogens is ethanol. The Fetal Alcohol Syndrome (FAS) is characterized by growth deficiency, particular facial features, and central nervous system (CNS) dysfunctions (mental retardation, microencephaly and brain malformations). Abuse of toluene by pregnant women can lead to an embryopathy (fetal solvent syndrome, (FSS)) whose characteristics are similar to FAS. Phenylketonuria (PKU) is a genetic defect in phenylalanine (Phe) metabolism. Offspring of phenylketonuric mothers not under strict dietary control are born with maternal PKU (mPKU), a syndrome with similar characteristics as FAS and FSS. While ethanol has been shown to cause neuronal death, no such evidence is available for toluene or Phe and/or its metabolites. On the other hand, alterations in astrocyte proliferation and maturation have been found, mostly in in vitro studies, which may represent a potential common mode of action for at least some of the CNS effects found in FAS, mPKU, and FSS. Further in vivo and in vitro studies should validate this hypothesis and elucidate possible molecular targets.
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PMID:Developmental neurotoxicity: do similar phenotypes indicate a common mode of action? A comparison of fetal alcohol syndrome, toluene embryopathy and maternal phenylketonuria. 1205 59

Behavioral phenotypes were studied in four mental retardation syndromes using the Developmental Behavior Checklist (DBC). The four samples comprised fetal alcohol syndrome (FAS), Prader-Willi syndrome (PWS), fragile X syndrome (FRAX), and tuberosis sclerosis (TSC). Both on the item and the subscale level, there were clear behavioral differentiations across the four syndromes. FAS and FRAX proved to be most clearly differentiated from the other two samples, with PWS and TSC showing lower scores and less abnormal behavior profiles. Neither intelligence nor gender nor age contributed to variations in the number of behavior abnormalities. It was concluded that the DBC as a quantitative approach contributes significantly to the differentiation of behavioral phenotypes in various mental retardation syndromes.
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PMID:Behavioral phenotypes in four mental retardation syndromes: fetal alcohol syndrome, Prader-Willi syndrome, fragile X syndrome, and tuberosis sclerosis. 1221 Feb 96


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