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Respir Physiol Neurobiol. 2013 Nov 1;189(2):301-14. doi: 10.1016/j.resp.2013.07.001. Epub 2013 Jul 10.

Serotonin gene variants are unlikely to play a significant role in the pathogenesis of the sudden infant death syndrome.

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  • 1Department of Pathology, Enders Building Room 1109, Boston Children's Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA 02115, United States. Electronic address:


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.

Copyright © 2013 Elsevier B.V. All rights reserved.

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