title: Serotonin gene variants are unlikely to play a significant role in the pathogenesis of the sudden infant death syndrome.
abstract: Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant less than 12 months of age that is related to a sleep period and remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. The cause of SIDS is unknown, but a major subset of SIDS is proposed to result from abnormalities in serotonin (5-HT) and related neurotransmitters in regions of the lower brainstem that result in failure of protective homeostatic responses to life-threatening challenges during sleep. Multiple studies have implicated gene variants that affect different elements of 5-HT neurotransmission in the pathogenesis of these abnormalities in SIDS. In this review I discuss the data from these studies together with some new data correlating genotype with brainstem 5-HT neurochemistry in the same SIDS cases and conclude that these gene variants are unlikely to play a major role in the pathogenesis of the medullary 5-HT abnormalities observed in SIDS.
authors.affiliation: Department of Pathology, Enders Building Room 1109, Boston Children's Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA 02115, United States. Electronic address: david.paterson@childrens.harvarvd.edu.
authors.forename: David S
authors.initials: DS
authors.lastname: Paterson
mesh_terms: D014644:Genetic Variation / Q000235:genetics* / Q000502:physiology; D006801:Humans; D007223:Infant; D009415:Nerve Net / Q000502:physiology; D011985:Receptors, Serotonin / Q000235:genetics*; D012307:Risk Factors; D012701:Serotonin / Q000235:genetics*; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D013398:Sudden Infant Death / Q000175:diagnosis* / Q000235:genetics*
chemical_list: D011985:Receptors, Serotonin; D050486:Serotonin Plasma Membrane Transport Proteins; D012701:Serotonin