@article{2998849,
    title = "Fetal alcohol spectrum disorders and cognitive functions of young children",
    author = "Bakoyiannis, I. and Gkioka, E. and Pergialiotis, V. and Mastroleon, I. and Prodromidou, A. and Vlachos, G.D. and Perrea, D.",
    journal = "Reviews in the Neurosciences",
    year = "2014",
    volume = "25",
    number = "5",
    pages = "631-639",
    publisher = "Walter de Gruyter GmbH",
    issn = "0334-1763, 2191-0200",
    doi = "10.1515/revneuro-2014-0029",
    keywords = "antioxidant;  neurotransmitter, Article;  child;  clinical feature;  cognition;  cognitive defect;  epigenetics;  fetal alcohol syndrome;  glycosylation;  human;  hypothalamus hypophysis adrenal system;  insulin resistance;  nonhuman;  oxidative stress;  pathogenesis;  pathophysiology;  United States;  animal;  Fetal Alcohol Spectrum Disorders;  genetic epigenesis;  genetics;  hypophysis adrenal system;  hypothalamus hypophysis system;  metabolism;  synaptic transmission, Animals;  Child;  Cognition;  Epigenesis, Genetic;  Fetal Alcohol Spectrum Disorders;  Glycosylation;  Humans;  Hypothalamo-Hypophyseal System;  Insulin Resistance;  Oxidative Stress;  Pituitary-Adrenal System;  Synaptic Transmission",
    abstract = "Fetal alcohol spectrum disorder (FASD) is one of the main causes of mental retardation worldwide. Nearly 1% of children in North America are affected from antenatal exposure to ethanol. Its economic burden in industrialized countries is increasing. It is estimated that, in the United States, 4.0 billion dollars are annually expended in the treatment and rehabilitation of these patients. As a pathologic entity, they present with a broad symptomatology. Fetal alcohol syndrome (FAS) is the most readily recognized clinical manifestation of these disorders. Various factors seem to contribute in the pathogenesis of FASD-related cognitive disorders. During the last 20 years, several potential pretranslational and posttranslational factors have been extensively studied in various experimental animal models. Research has specifically focused on several neurotransmitters, insulin resistance, alterations of the hypothalamic-pituitary-adrenal (HPA) axis, abnormal glycosylation of several proteins, oxidative stress, nutritional antioxidants, and various epigenetic factors. The purpose of the present review is to summarize the clinical manifestations of this disorder during childhood and adolescence and to summarize the possible pathophysiologic and epigenetic pathways that have been implicated in the pathophysiology of FASD. © 2014 by De Gruyter."
}