Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of the fetal central nervous system can be effected by drugs. In this paper we review the neurological consequences of intrauterine exposure to alcohol, cocaine, opiates and marijuana. Ethanol causes the fetal alcohol syndrome: mental retardation, intrauterine and postnatal growth retardation, and peculiar dysmorphic features. Is pathogenesis has been explained on the basis of maternal nutritional deficiencies or due to abnormalities in the conversion of ethanol to aldehyde, or abnormalities in the metabolism of prostaglandins or retinoic acid, the neurotransmitter systems, the neuronal excitotoxic activity, the development of the white matter, the production of gangliosides, and/or genetic regulation cell-cell adhesion. Cocaine has been related to congenital malformations, neurologic abnormalities during the neonatal period and psychomotor and cognitive development deficits. Characteristic dysmorphic features and a higher incidence of the sudden infant death syndrome (SIDS) have also been described. The following mechanisms have been implicated in the pathogenesis: vascular effects, superoxide formation, chelation of calcium ion channels, and abnormalities in the production of glycosphingolipids, the synthesis of DNA, the functioning of neurotransmitter systems, the neuronal growth and differentiation, the neuronal excitotoxic activity and/or the expression of early immediate genes. Opiates produce intrauterine and postnatal growth retardation, neonatal abstinence syndrome, and deficits of the psychomotor and cognitive development. They also increase the incidence of SIDS. The pathogenesis has been related to abnormalities in the sensitivity of the locus ceruleus, the functioning of the neurotransmitter systems, and/or the expression of early immediate genes. Marijuana has been associated with intrauterine growth retardation, dysmorphic features, and abnormalities of the behavior during the neonatal period, the psychomotor and cognitive development, and the sleep. The pathogenesis is thought to be due to an action upon specific receptors, or upon the neurotransmitter systems, and/or to an increase in the production of carbon monoxide. The best treatment of the syndrome of intrauterine exposure to drugs in the prophylaxis. The identification of emotional and drug addiction problems in the mother can avoid disastrous consequences. The care of these children is complex and requires a good pediatric follow-up and an early intervention program while the mother on the parents continue with the drug addiction therapy. The coordinations of all the necessary services with the active participation of social workers, physicians, educators and teachers is crucial for a successful treatment.
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PMID:[Intrauterine exposure to drugs]. 920 93

Women at childbearing age often use alcohol and various illicit drugs such as cocaine and heroin. These agents pass through the human placenta and may affect the developing embryo and fetus. Indeed, large amounts of alcohol ingested by the pregnant woman may produce a specific syndrome manifested by prenatal and postnatal growth retardation, a variety of facial dysmorphic features and mental retardation. Ingestion of smaller amounts of alcohol will produce the fetal alcohol effects with only few and minor dysmorphic features but with developmental delay and some degree of intellectual impairment. Cocaine use during pregnancy may apparently result in an increase in the rate of congenital anomalies, of stillbirth and of intrauterine growth retardation. The use of heroin and opiates does not seem to increase the rate of major congenital anomalies, but it reduces fetal growth and increases the rate of intrauterine fetal death. Studies on the developmental outcome of children born to cocaine or heroin dependent mothers seem all to show psychomotor developmental delay at a young age. At school age these children have intellectual impairment and a very high rate of inattention and/or hyperactivity. We should therefore address our efforts in improving the environment of these children and in treating the early symptoms of inattention and hyperactivity, even before the child reaches school.
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PMID:The effects of alcohol and illicit drugs on the human embryo and fetus. 1222 27

Substance abuse in pregnancy has increased over the past three decades in the United States, resulting in approximately 225,000 infants yearly with prenatal exposure to illicit substances. Routine screening and the education of women of child bearing age remain the most important ways to reduce addiction in pregnancy. Legal and illegal substances and their effect on pregnancy discussed in this review include opiates, cocaine, alcohol, tobacco, marijuana, and amphetamines. Most literature regarding opiate abuse is derived from clinical experience with heroin and methadone. Poor obstetric outcomes can be up to six times higher in patients abusing opiates. Neonatal care must be specialized to treat symptoms of withdrawal. Cocaine use in pregnancy can lead to spontaneous abortion, preterm births, placental abruption, and congenital anomalies. Neonatal issues include poor feeding, lethargy, and seizures. Mothers using cocaine require specialized prenatal care and the neonate may require extra supportive care. More than 50% of women in their reproductive years use alcohol. Alcohol is a teratogen and its effects can include spontaneous abortion, growth restriction, birth defects, and mental retardation. Fetal alcohol spectrum disorder can have long-term sequelae for the infant. Tobacco use is high among pregnant women, but this can be a time of great motivation to begin cessation efforts. Long-term effects of prenatal tobacco exposure include spontaneous abortion, ectopic pregnancy, placental insufficiency, low birth weight, fetal growth restriction, preterm delivery, childhood respiratory disease, and behavioral issues. Marijuana use can lead to fetal growth restriction, as well as withdrawal symptoms in the neonate. Lastly, amphetamines can lead to congenital anomalies and other poor obstetric outcomes. Once recognized, a multidisciplinary approach can lead to improved maternal and neonatal outcomes.
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PMID:Addiction in pregnancy. 2040 75

Cocaine is a psychostimulant whose abuse causes a social and economic burden for our society. Most of the published literature deals with acute effects of cocaine or short-term abstinence in adult animals but much less information exists on neuroplastic changes following long-term abstinence. We have recently shown that the long-term abstinence following developmental exposure to cocaine results in increased Activity-Regulated Cytoskeletal-associated protein (Arc/Arg3.1) expression in the crude synaptosomal fraction (Giannotti et al. Int J Neuropsychopharmacology 7(4):625-634, 2014). Given that Arc/Arg3.1 localizes not only at active synapse but also in the nucleus (Okuno et al. Cell 149:886-898, 2012; Korb et al. Nat Neurosci 16:874-883 2013; Bloomer et al. Brain Res 1153:20-33 2007), we investigated Arc/Arg3.1 protein levels in the whole homogenate and the nuclear fraction of animals exposed to cocaine during adolescence. We observed the increased expression of Arc/Arg3.1 in both the fractions, suggesting that up-regulation of Arc/Arg3.1 protein may be partly due to the increased nuclear expression of Arc/Arg3.1 in the medial prefrontal cortex (mPFC) of rats sacrificed at postnatal day 90, following 48 days of abstinence. This effect seems to cause reduced Gria1 transcription. We also found reduced expression of fragile X mental retardation gene (FMR1) which normally inhibits Arc/Arg3.1 translation together with reduced expression of Ubiquitin-protein ligase E3A (Ube3a) that normally causes Arc/Arg3.1 protein degradation via ubiquitination. Further, we found increased expression of metabotropic glutamate receptor 5 (GRM5) which is also involved in the regulation of Arc/Arg3.1 expression. Taken together, our findings show that abstinence from developmental exposure to cocaine is associated with alterations in the finely tuned mechanisms that regulate Arc/Arg3.1 expression.
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PMID:Long-term abstinence from developmental cocaine exposure alters Arc/Arg3.1 modulation in the rat medial prefrontal cortex. 2481 Jun 62