Mechanisms of brain injury: L1 cell adhesion molecule as a target for ethanol-induced prenatal brain injury.
The magnitude of the problem of neurodevelopmental disorders is enormous. Frequently, the mechanism of injury is unknown. In this article, the function of one cell adhesion molecule, L1, will be reviewed. L1 is critical for proper central nervous system development. Similarities between patients with fetal alcohol syndrome and with L1 mutations suggest that the mechanism of developmental neurotoxicity of ethanol is partly due to effects on L1 cell adhesion molecule.
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Case Western Reserve University, Cleveland, OH, USA.
D000328:Adult; D000954:Antigens, Surface / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D005314:Embryonic and Fetal Development / Q000187:drug effects; D000431:Ethanol / Q000009:adverse effects*; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000209:etiology / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D006801:Humans; D007231:Infant, Newborn; D039841:Leukocyte L1 Antigen Complex; D008562:Membrane Glycoproteins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D019006:Neural Cell Adhesion Molecules / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013723:Teratogens
D000954:Antigens, Surface; D039841:Leukocyte L1 Antigen Complex; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules; D013723:Teratogens; D000431:Ethanol