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A. Fainsod et al.
Analysis of ethanol effects and resulting FASD phenotypes has revealed a wide
spectrum of abnormalities extending from behavioral anomalies and anatomical malformations to epigenetic changes and cell death (Figs. 8.1 and 8.2). Several models have been proposed providing; molecular, biochemical, cellular, and embryonic
explanations for the induced developmental malformations in human and non-human
embryos and fetuses (Gilbert-Barness 2010; Caputo et al. 2016; Eberhart and Parnell
2016; Gupta et al. 2016; Kane and Drew 2016; Liu et al. 2016; Lunde et al. 2016;
Wells et al. 2016; Chater-Diehl et al. 2017; Davis-Anderson et al. 2017; Lussier
et al. 2017; Shenoda 2017; Tai et al. 2017; Kalisch-Smith and Moritz 2018; Mandal
et al. 2018; Shabtai and Fainsod 2018; Ehrhart et al. 2019). Since recent evidence has
accumulated linking the induction of FASD to reduced RA signaling during embryogenesis, this chapter will focus on the origin of the main developmental malformations of FASD in the context of RA “starvation”. Evidence from additional human
syndromes linked to the same signaling pathway is also described and discussed.
Fig. 8.1 Summary of the
main developmental
malformations associated
with Fetal Alcohol
Syndrome
Fig. 8.2 The main
behavioral anomalies and
mental disabilities
(neurological abnormalities)
induced by ethanol in FASD
patients