Cot death: can the answer be found in serotonin levels?
EU-funded researchers have found a possible link between SIDS (Sudden Infant Death Syndrome) and the serotonin levels of infants. Writing in the journal Science, they reveal that an imbalance of the neuronal signal serotonin in the brainstem is sufficient to cause sudden death in mice. The researchers hope their findings will help doctors to identify the babies most at risk of SIDS before it is too late. The cause of cot death has long been a mystery. Its more medical term, Sudden Infant Death Syndrome (SIDS) reflects this mystery, and is only applied to the sudden and unexpected death of an infant, the cause of which cannot be explained. Postmortem investigations have shown changes in serotonin neurons in the brainstem of infants of SIDS. What remained a mystery was the precise mechanism by which altered serotonin homeostasis might cause sudden death. In this latest study, researchers at the European Molecular Biology Laboratory (EMBL) Mouse Biology Unit in Monterotondo, Italy, studied a mouse model of SIDS. The group at the EMBL, led by Cornelius Gross, modified the serotonin system of mice. This modification gave the team a better understanding of the role of this signalling molecule in the brainstem. Initial results showed no changes in the behaviour of the mice. After a while however, the researchers witnessed drastic changes. 'At first sight the mice were normal. But then they suffered sporadic and unpredictable drops in heart rate and body temperature,' said Professor Gross. 'More than half of the mice eventually died of these crises during a restricted period of early life. It was at that point that we thought it might have something to do with SIDS,' he added. Previous research had hinted at the role that serotonin plays, but it remained unclear how changes in serotonin signalling in the brainstem of SIDS infants are involved in sudden death. What these findings show is that deficits in serotonin signalling in the brainstem can be sufficient to cause sudden death and strongly support the idea that a congenital serotonin defect could play a critical role in SIDS. Enrica Audero was also involved in the research. 'We hope the mouse model will help identify risk factors for SIDS. One open question is whether like in SIDS, the animals die during sleep and whether we can identify which mice will die by looking at their heart rate or body temperature before the crisis. Ultimately, we hope it will give new ideas to doctors about how to diagnose babies at risk for SIDS,' said Dr Audero. EU support for the research came from the NEWMOOD ('New molecules in mood disorders: a genomic, neurobiological and systems approach in animal models and human disorder') project, which is financed under the 'Life sciences, genomics and biotechnology for health' thematic area of the Sixth Framework Programme (FP6).