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      NGF and BDNF Alterations by Prenatal Alcohol Exposure

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          Abstract

          Background

          It is now widely established that the devastating effects of prenatal alcohol exposure on the embryo and fetus development cause marked cognitive and neurobiological deficits in the newborns. The negative effects of the gestational alcohol use have been well documented and known for some time. However, also the subtle role of alcohol consumption by fathers prior to mating is drawing special attention.

          Objective

          Both paternal and maternal alcohol exposure has been shown to affect the neurotrophins' signalling pathways in the brain and in target organs of ethanol intoxication. Neurotrophins, in particular nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by alcohol exposure.

          Methods

          New researches from the available literature and experimental data from our laboratory are presented in this review to offer the most recent findings regarding the effects of maternal and paternal prenatal ethanol exposure especially on the neurotrophins' signalling pathways.

          Results

          NGF and BDNF changes play a subtle role in short- and long-lasting effects of alcohol in ethanol target tissues, including neuronal cell death and severe cognitive and physiological deficits in the newborns.

          Conclusion

          The review suggests a possible therapeutic intervention based on the use of specific molecules with antioxidant properties in order to induce a potential prevention of the harmful effects of the paternal and/or maternal alcohol exposure.

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          Most cited references111

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          Estimation of national, regional, and global prevalence of alcohol use during pregnancy and fetal alcohol syndrome: a systematic review and meta-analysis.

          Alcohol use during pregnancy is the direct cause of fetal alcohol syndrome (FAS). We aimed to estimate the prevalence of alcohol use during pregnancy and FAS in the general population and, by linking these two indicators, estimate the number of pregnant women that consumed alcohol during pregnancy per one case of FAS.
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            Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.

            The deleterious effects of ethanol on the developing human brain are poorly understood. Here it is reported that ethanol, acting by a dual mechanism [blockade of N-methyl-D-aspartate (NMDA) glutamate receptors and excessive activation of GABA(A) receptors], triggers widespread apoptotic neurodegeneration in the developing rat forebrain. Vulnerability coincides with the period of synaptogenesis, which in humans extends from the sixth month of gestation to several years after birth. During this period, transient ethanol exposure can delete millions of neurons from the developing brain. This can explain the reduced brain mass and neurobehavioral disturbances associated with human fetal alcohol syndrome.
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              Prevalence and epidemiologic characteristics of FASD from various research methods with an emphasis on recent in-school studies.

              Researching the epidemiology and estimating the prevalence of fetal alcohol syndrome (FAS) and other fetal alcohol spectrum disorders (FASD) for mainstream populations anywhere in the world has presented a challenge to researchers. Three major approaches have been used in the past: surveillance and record review systems, clinic-based studies, and active case ascertainment methods. The literature on each of these methods is reviewed citing the strengths, weaknesses, prevalence results, and other practical considerations for each method. Previous conclusions about the prevalence of FAS and total FASD in the United States (US) population are summarized. Active approaches which provide clinical outreach, recruitment, and diagnostic services in specific populations have been demonstrated to produce the highest prevalence estimates. We then describe and review studies utilizing in-school screening and diagnosis, a special type of active case ascertainment. Selected results from a number of in-school studies in South Africa, Italy, and the US are highlighted. The particular focus of the review is on the nature of the data produced from in-school methods and the specific prevalence rates of FAS and total FASD which have emanated from them. We conclude that FAS and other FASD are more prevalent in school populations, and therefore the general population, than previously estimated. We believe that the prevalence of FAS in typical, mixed-racial, and mixed-socioeconomic populations of the US is at least 2 to 7 per 1,000. Regarding all levels of FASD, we estimate that the current prevalence of FASD in populations of younger school children may be as high as 2-5% in the US and some Western European countries. (c) 2009 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Curr Neuropharmacol
                Curr Neuropharmacol
                CN
                Current Neuropharmacology
                Bentham Science Publishers
                1570-159X
                1875-6190
                April 2019
                April 2019
                : 17
                : 4
                : 308-317
                Affiliations
                Institute of Cell Biology and Neurobiology (IBCN-CNR) , Rome, , Italy; Center for Alcohol Abuse (Centro Riferimento Alcologico Regione Lazio-CRARL), Department of Clinical Medicine, Sapienza University of Rome , Italy; Department of Cellular Biotechnologies and Hematology, Sapienza University of Rome , Italy; Institute of Translational Pharmacology, (IFT-CNR), Rome, , Italy
                Author notes
                [* ]Address correspondence to this author at the Istituto di Biologia Cellulare e Neurobiologia, Consiglio Nazionale delle Ricerche (CNR), via del Fosso di Fiorano 64, 00143 Roma, Italy; Tel: +3906501703239;, Fax: +3906501703313; E-mail: marco.fiore@ 123456cnr.it
                Article
                CN-17-308
                10.2174/1570159X15666170825101308
                6482479
                28847297
                7e0c266f-c918-48d9-8ec5-9edc0a025c25
                © 2019 Bentham Science Publishers

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 28 June 2017
                : 02 August 2017
                : 20 August 2017
                Categories
                Article

                Pharmacology & Pharmaceutical medicine
                gestational alcohol,fas,oxidative stress,fasd,ngf,bdnf
                Pharmacology & Pharmaceutical medicine
                gestational alcohol, fas, oxidative stress, fasd, ngf, bdnf

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