Experimental Models of Early Exposure to Alcohol: A Way to Unravel the Neurobiology of Mental Retardation

摘要

As of November 2014, a PubMed search for “fetal alcohol” retrieved more than 14,500 articles. Alcohol consumption during pregnancy and its detrimental consequences on the developing brain raise major public health, social, and economic issues. However, the research on fetal alcohol spectrum disorders (FASD) in the real world is challenging, given that it is largely based on retrospective analysis. Therefore, establishing the relationship between brain damage and drinking habits proves particularly hard. One of the advantages of FASD studies carried out in the laboratory environment derives from the tight control of time, dose, and modality of alcohol exposure (1). Furthermore, since FASD are among the leading causes of intellectual disability, animal models of early exposure to alcohol represent an invaluable tool to elucidate the basic neurobiological mechanisms leading to the cognitive defects. Experimental models of genetic syndromes are ideally suited to study the role of single molecules, such as the fragile X mental retardation protein, throughout the maturation of the nervous system. Conversely, experimental exposure to alcohol can be carried out during discrete, often very restricted, time windows and, though depending on the interference with several molecular pathways, can provide information about which developmental periods and brain areas are critically involved in the genesis of the intellectual disability.