Low serotonin levels in brain associated with SIDS.
Decreased levels in the brainstem of serotonin (5-HT--a chemical that helps to regulate breathing, blood pressure and heart rate in the brain during sleep) and tryptophan hydroxylase (TPH2--an enzyme involved in the synthesis of serotonin) are associated with an increased risk for sudden infant death syndrome (SIDS), researchers have concluded. SIDS is believed to result from abnormalities in brainstem control of autonomic function and breathing during a critical developmental period. Abnormalities of serotonin in regions of the medulla oblongata involved in this control have been reported in infants who have died from SIDS. To test the hypothesis that SIDS is associated with reductions in tissue levels of 5-HT, TPH2 or both, US researchers conducted a study to analyse levels of 5-HT and TPH2 in 41 infants who died from SIDS (cases), seven infants with acute death from known causes (controls) and five hospitalised infants with chronic hypoxiaischemia. 5-HT levels were 26% lower in regions of the brain of SIDS cases compared with controls, TPH2 levels were 22% lower in the SIDS cases compared with controls, and 5-HT levels were higher in the hospitalised group compared with the SIDS group. The authors conclude that compared with controls, SIDS was associated with lower 5-HT and TPH2 levels, consistent with a disorder of medullary 5-HT deficiency.
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|Title Annotation:||sudden infant death syndrome|
|Date:||Mar 1, 2010|
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