Mechanisms of ethanol-induced degeneration in the developing, mature, and aging cerebellum
Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders  (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by preand postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system  (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation , when the neural tube  is formed, all the way through to birth. The cerebellum  is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction  in brain cells include apoptosis , oxidative stress, and damage to the radial glia  stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning  tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.