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Prenatal alcohol exposure has been directly implicated in a wide range of deficits that adversely influence the development of affected individuals. Fetal Alcohol Spectrum Disorder (FASD) is an umbrella term referring to a continuum of effects that occur in individuals who were prenatally exposed to alcohol. FASD is a permanent birth defect, and a leading cause of mental retardation and developmental delay. This book gathers the latest research in the study of pregnancy and alcohol consumption from authors around the globe, including the biochemistry of prenatal alcohol exposure; research on interventions to prevent alcohol consumption during pregnancy; medico-legal considerations concerning foetal alcohol spectrum disorders; life as an adult with foetal alcohol syndrome; and biological markers of exposure of the foetus to alcohol during pregnancy.
Women drinking during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which may feature variable neurodevelopmental deficits, facial dysmorphology, growth retardation, and learning disabilities. Research suggests the human brain is precisely formed through an intrinsic, genetic-cellular expression that is carefully orchestrated by an epigenetic program. This program can be influenced by environmental inputs such as alcohol. Current research suggests the genetic and epigenetic elements of FASD are heavily intertwined and highly dependent on one another. As such, now is the time for investigators to combine genetic, genomic and epigenetic components of alcohol research into a centralized, accessible platform for discussion. Genetic analyses inform gene sets which may be vulnerable to alcohol exposure during early neurulation. Prenatal alcohol exposure indeed alters expression of gene subsets, including genes involved in neural specification, hematopoiesis, methylation, chromatin remodeling, histone variants, eye and heart development. Recently, quantitative genomic mapping has revealed loci (QTLs) that mediate alcohol-induced phenotypes identified between two alcohol-drinking mouse strains. One question to consider is (besides the role of dose and stage of alcohol exposure) why only 5% of drinking women deliver newborns diagnosed with FAS (Fetal Alcohol Syndrome)? Studies are ongoing to answer this question by characterizing genome-wide expression, allele-specific expression (ASE), gene polymorphisms (SNPs) and maternal genetic factors that influence alcohol vulnerability. Alcohol exposure during pregnancy, which can lead to FASD, has been used as a model to resolve the epigenetic pathway between environment and phenotype. Epigenetic mechanisms modify genetic outputs through alteration of 3D chromatin structure and accessibility of transcriptional machinery. Several laboratories have reported altered epigenetics, including DNA methylation and histone modification, in multiple models of FASD. During development DNA methylation is dynamic yet orchestrated in a precise spatiotemporal manner during neurulation and coincidental with neural differentiation. Alcohol can directly influence epigenetics through alterations of the methionine pathway and subsequent DNA or histone methylation/acetylation. Alcohol also alters noncoding RNA including miRNA and transposable elements (TEs). Evidence suggests that miRNA expression may mediate ethanol teratology, and TEs may be affected by alcohol through the alteration of DNA methylation at its regulatory region. In this manner, the epigenetic and genetic components of FASD are revealing themselves to be mechanistically intertwined. Can alcohol-induced epigenomic alterations be passed across generations? Early epidemiological studies have revealed infants with FASD-like features in the absence of maternal alcohol, where the fathers were alcoholics. Novel mechanisms for alcohol-induced phenotypes include altered sperm DNA methylation, hypomethylated paternal allele and heritable epimutations. These studies predict the heritability of alcohol-induced epigenetic abnormalities and gene functionality across generations. We opened a forum to researchers and investigators the field of FASD to discuss their insights, hypotheses, fresh data, past research, and future research themes embedded in this rising field of the genetics and epigenetics of FASD. This eBook is a product of the collective sharing and debate among researchers who have contributed or reviewed each subject.
This report details our progress during the second year of a three-year proposal. The proposal's overall goal is to uncover biochemical mechanisms that underlie learning and memory deficits resulting from fetal alcohol exposure (FAE). We have made three important novel observations: First, we found that FAE increases the amount of PLC activity associated with extracellular signal-regulated kinase 2 (ERK2) in the hippocampal formation isolated from control animals. Second, we found that FAE modifies the effect of fear conditioning on the association between ERK2 and phospholipase C (PLC). Third, we identified that ERK2 associates with PLC-beta and PLC-gamma isozymes in rat hippocampal formation. Finally, we have initiated studies on the effect of ERK2-dependent phosphorylation on of PLC on PLC enzyme activity. In addition to increasing our understanding of the biochemical basis of FAE-induced learning deficits, the next phase of these studies is expected to yield important information about the neurochemical mechanisms that underlie fear and stress, and, consequently, may provide insight into the neurochemical basis of posttraumatic stress syndrome.
The neurological consequences of alcohol abuse need additional research concentrating on prevention and treatment. Public attention and research efforts are being driven by an ever- increasing understanding of the problems and magnitude of alcohol on neurological development. The 10 million alcohol-abusing adults, along with unborn children exposed to alcohol in utero, cost the people of the U.S. more than $100 billion in lost wages, health care, theft, damaged mental functions, and shortened life span. An intimate, detailed knowledge of the effects of alcohol on the biochemical reactions and neurological changes is critical in preventing or treating abuse. We must study the mechanisms of ethanol's effects on the neurological system at a cellular and systematic level to understand its action. These include modifications of hormonal regulation and production with its major functional consequences. Brain development including its cells are a major focus and emphasis of this volume. The progress of research over the past decade is encouraging as we begin to summarize and evaluate in detail advances in understanding changes in the brain's biochemistry and physiology caused by ethanol. This information will assist the researcher, clinician, and student in comprehending the complex changes caused by direct and indirect effects of single drugs at the cellular level.
The Novartis Foundation Series is a popular collection of the proceedings from Novartis Foundation Symposia, in which groups of leading scientists from a range of topics across biology, chemistry and medicine assembled to present papers and discuss results. The Novartis Foundation, originally known as the Ciba Foundation, is well known to scientists and clinicians around the world.
This eBook addresses the impact of prenatal exposure to alcohol, and Fetal Alcohol Spectrum Disorders (FASD). It presents a compilation of current research by leading experts in the field and serves as a guide to future directions in FASD research, interventions and treatment. the book includes a comprehensive compendium of our knowledge of the dangers of prenatal alcohol exposure and covers ways to screen and intervene with pregnant women, diagnosis and treatment to ameliorate the effects of prenatal alcohol exposure (through the lifespan), and other related issues, such as building a state infrastructure of health services and legislation. the eBook is intended as a textbook for graduate courses relevant to FASD.
My initial purpose in writing this book was to offer readers an update of my book Fetal Alcohol Syndrome and Fetal Alcohol Effects (Plenum, 1984), which con tained a broad overview of the history (actually the absence of any history) ofthe awareness of alcohol's teratogenic potential; a review of alcohol's pharmacology, especially with respect to pregnancy; a survey of the physical and behavioral effects of prenatal alcohol exposure; and an overview of the mechanisms sus pected of being responsible for those effects. I have omitted most of the previously examined historical and pharmacologi cal information because not much of what was previously discussed needed revision. On the other hand, because much more has been learned about the consequences of prenatal alcohol exposure and its potential mechanisms of action, I have considerably expanded my discussion of these topics. In doing so, I have attempted to include as much new material as possible without (I hope) being overly pedantic and thereby losing the proverbial forest for the trees. No book is ever entirely neutral in the topics it discusses, the issues it raises, or in its conclusions. In sifting through hundreds and oftentimes thousands of articles, writers have to choose which facts to emphasize and which to ignore. Every idea cannot be chronicled and every article cannot (and should not) be cited. In going about the business of picking and choosing, however, a writer has an obligation to present the arguments for and against a particular conclusion.
Recognition of the relationship between alcohol abuse and adverse prenatal outcomes is reflected in the warning labels on every alcoholic beverage sold in the United States. Because alcohol abuse has serious consequences for both individuals and society as a whole, much research has been devoted to this problem. Fetal Alcohol Syndrome provides straightforward facts regarding the impact of alcohol consumption as it affects the development of the embryo and fetus. Surveying current research of fetal alcohol syndrome and its related problems, the book addresses the immediate effects on development at various stages. Long-term action of prenatal alcohol exposure later in life is also considered. A chapter devoted to assessing the behavior of children who were prenatally exposed to alcohol emphasizes the necessity of longitudinal studies of fetal alcohol syndrome. This important reference offers a thorough overview of a problem that cannot be ignored.