Prenatal alcohol (ethanol) exposure can have dramatic effects on the development of the central nervous system (CNS), including morphological abnormalities and an overall reduction in white matter of the brain. The impact of ethanol on neural stem cells such as radial glia (RG) has proven to be a significant cause of these defects, interfering with the creation and migration of neurons and glial cells during development. The impact of ethanol on RG can occur as early as three weeks after fertilization and can persist through the third trimester of pregnancy, interfering with intrinsic mechanisms and signaling pathways to impede cellular proliferation, differentiation, and survival.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical and neurological developmental abnormalities that vary depending on the timing, duration, and degree of alcohol exposure. Heavy exposure during development may lead to the condition Fetal Alcohol Syndrome (FAS), characterized by growth deficits, neurological deficiencies and minor facial abnormalities. Alcohol is a known teratogen, an agent that causes birth defects and acts upon developing embryos through mechanisms that are not yet fully understood. One of the better understood developmental effects of alcohol relates to the minor facial abnormalities associated with FAS, particularly the role that the gene sonic hedgehog (shh) plays in the regulation of craniofacial defects. In comparative animal studies, maternal exposure to alcohol results in the massive decrease of shh and shh transcription factors in affected cell populations. However, the exogenous application of shh to the developing embryo has shown limited success in reversing this expression, thereby restoring a normative pattern of craniofacial development in the affected embryo.