The serotonergic network and SIDS

Cot death or Sudden Infant Death Syndrome (SIDS) is fortunately a rare phenomenon. Still it makes up a measurable fraction of the annual deaths among children up to the age of three, since the mortality rate in this age group is low. The shock is also that much worse when a seemingly healthy child suddenly dies. For several decades one has tried to find factors that can trigger and predispose to this condition. Research groups in the US, Japan and Norway among others have conducted research on a cellular and molecular level in affected infants. The scope has not yet been limited to one field only, but most researches base their investigations on a principle proposed by R.J. Wedgewood in 1970, the triple-risk hypothesis. Here he proposes that an infant exposed to an external risk factor, with a genetic predisposition and at a vulnerable stage in development is at risk of SIDS. The external risk factors are fairly well mapped out. Mothers are advised not to smoke during pregnancy, and parents told to take care when co-sleeping and to avoid the prone sleeping position when putting the child to sleep. The vulnerable stage refers to the development of regulatory functions of the nervous system such as breathing, alertness and consciousness, and development of the immune system. The most controversial part of the hypothesis is the genetic predisposition, and this review will discuss some of the studies made on genetic polymorphisms (variants of genes found in the population), more specifically the 5-HT (serotonin) related polymorphisms. During the last two decades researchers have found anatomical discrepancies in the brainstem of infants affected by SIDS and described several polymorphisms related to the serotonergic network in the brainstem of SIDS victims