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#FAS

2 public questions tagged with this topic.

Teratogens

Fetal Alcohol Syndrome (FAS) primarily results from damage to:

Facial dysmorphology and microcephaly hallmark fetal alcohol syndrome originate primarily from injury to two populations. Cranial neural crest cells arising at dorsal neural tube edges migrate into frontonasal prominence contributing to facial skeleton highly sensitive to oxidative apoptosis, impaired L1 adhesion and reduced sonic hedgehog trophic support after ethanol. Depleted crest leads to midfacial hypoplasia. Simultaneously ventricular zone neuronal progenitors and postmitotic neurons undergo ROS-mediated apoptosis and cell cycle arrest, reducing brain volume and cortical complexity. Liver, lung less affected. Combined neural crest and neuronal cell loss explains neurocristopathy features central to fetal alcohol syndrome presentation.

Ref: Moore, The Developing Human, 11th ed., Chapter 20: FAS neural crest and neuronal damage.

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Teratogens

Alcohol exposure during pregnancy causes defects similar to human FAS in:

Developmental toxicology testing for fetal alcohol spectrum relies on mammalian placental models recapitulating ethanol metabolism via alcohol dehydrogenase, generation of acetaldehyde, reactive oxygen species and pharmacokinetics comparable to human exposure. Mice exhibit craniofacial features resembling human fetal alcohol syndrome including midfacial hypoplasia, micrognathia, growth retardation and neurobehavioral deficits following gestational ethanol dosing during gastrulation or organogenesis. Genetic tractability allows investigation of L1CAM adhesion, Sonic hedgehog interaction. While rats show similar effects, mice provide best characterized mammalian system demonstrating human-like FAS defects following prenatal alcohol exposure.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: Alcohol teratogenesis mouse FAS model.

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