Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (11): 1764-1766.doi: 10.4103/1673-5374.165290

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Fetal alcohol spectrum disorder: molecular insights into neural damage reduction

Diana Le Duc*   

  1. Institute of Biochemistry, Molecular Biochemistry, Medical Faculty, University of Leipzig, Johannisallee 30, 04103 Leipzig, Germany
  • Received:2015-07-31 Online:2015-12-07 Published:2015-12-07
  • Contact: Diana Le Duc, Ph.D.,Gabriela-Diana.LeDuc@medizin.uni-leipzig.de;Diana_leduc@eva.mpg.de.

Abstract:

Fetal Alcohol Spectrum Disorders (FASD) is a group of entirely preventable, lifelong conditions, which occur upon maternal alcohol use during pregnancy. This can result in severe consequences for the newborn and ultimately the family. It is usually characterized by delays in development and motor function, craniofacial abnormalities, and difficulties with learning, memory, speech, and academic achievement. According to the German guidelines for fetal alcohol syndrome (FAS) diagnosis, the prevalence of FASD ranges between 0.02–0.8% of all annual births and often the disorder is not recognized. The U.S. National Institutes of Health regard FAS as the most common nonhereditary cause of mental retardation. Thus, preventing programs, like the one undertaken by the Australian Government, which appointed a National FASD Technical Network, may seem a very reasonable strategy. However, preventing programs for FASD focus mainly either on primary prevention, by increasing pregnant women’s awareness of ethanol consumption risks, or on tertiary prevention which supposes early recognition of the condition and social support in the form of an improved developmental framework of the affected individual. Secondary prevention of the disorder, which includes early detection by screening and treatment of the pre clinical pathological conditionis considered to be most challenging. This form of prevention could prove useful in the treatment and control of FAS progression, but therapy approaches are hindered by our limited knowledge of molecular mechanisms responsible for neuronal damage.