Abstract
Fetal alcohol spectrum disorder (FASD), caused by prenatal alcohol exposure, can result in craniofacial dysmorphism, cognitive impairment, sensory and motor disabilities among other defects. FASD incidences are as high as 2% to 5 % children born in the US, and prevalence is higher in low socioeconomic populations. Despite various mechanisms being proposed to explain the etiology of FASD, the molecular targets of ethanol toxicity during development are unknown. Proposed mechanisms include cell death, cell signaling defects and gene expression changes. More recently, the involvement of several other molecular pathways was explored, including non-coding RNA, epigenetic changes and specific vitamin deficiencies. These various pathways may interact, producing a wide spectrum of consequences. Detailed understanding of these various pathways and their interactions will facilitate the therapeutic target identification, leading to new clinical intervention, which may reduce the incidence and severity of these highly prevalent preventable birth defects. This review discusses manifestations of alcohol exposure on the developing central nervous system, including the neural crest cells and sensory neural placodes, focusing on molecular neurodevelopmental pathways as possible therapeutic targets for prevention or protection.
Highlights
Fetal alcohol syndrome (FAS), which affects approximately 2 to 7 of 1000 live births, is a severe developmental deficit caused by maternal ingestion of ethanol during pregnancy
Studies conducted in different animal models, in mice, that recapitulate a similar spectrum of brain and facial malformations upon alcohol exposure provided strong evidence that alcohol induced these craniofacial alterations [4,5,6,7,8]
To identify the olfactory developmental mechanisms disrupted by fetal alcohol exposure in more detail [37], gene chip experiments showed reduced expression of the metabotropic glutamate receptor 2 gene which are expressed by the olfactory sensory neurons (OSNs) and M/T cells
Summary
Fetal alcohol syndrome (FAS), which affects approximately 2 to 7 of 1000 live births, is a severe developmental deficit caused by maternal ingestion of ethanol during pregnancy. Affected individuals exhibit a spectrum of defects including specific physical, cognitive, psychomotor, behavioral, and learning disabilities with identifiable facial dysmorphology. Many more affected subjects are not readily identifiable by the facial features This previously undiagnosed population is estimated as high as ten times that of FAS and is categorized as fetal alcohol spectrum disorders (FASD) [1]. A significant amount of research work was done since FAS was defined in 1973 to understand alcohol’s teratogenic effect during development. It is still not clear how alcohol consumption produces a wide spectrum of physical and mental disabilities.
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