中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (11): 1764-1766.doi: 10.4103/1673-5374.165290

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

分子学洞察胎儿酒精综合症的神经元损伤 

  

  • 收稿日期:2015-07-31 出版日期:2015-12-07 发布日期:2015-12-07

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.

摘要:

母亲在妊娠期间酗酒,酒清会进入胎盘,阻碍胎儿的成长,破坏神经元及脑部结构,引起身体、心智及行为问题。发病率每年为0.02-0.8%。该篇观点文章表示,预防被证明在胎儿酒精中毒综合征进展的治疗和控制过程中是有用的,但是治疗方法却受限于我们对神经元损伤分子机制的有限认识。Bosco和Diaz首次提出这种假设,即缺氧和氧化应激可增强与胎儿发育延迟以及胎儿酒精中毒综合症有关。

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.