14 DAY TRIAL // Sudden infant death syndrome, also known as cot death in certain areas of the world, is a condition in which infant children up to several months of age die without warning, although not suffering of any serious known diseases. Cot death is largely mysterious even today, since there is no clear indication to what is triggering it. It is estimated that 1 in 2,000 born children eventually fall victim to cot death, making it the biggest cause of death in healthy newborns.
Lately, biologist Cornelius Gross of the European Molecular Biology Laboratory discovered that in mice cot death can be explained through an imbalance of the levels of serotonin in the brain. Perhaps further studying this would result in the creation of a model that would help predict which children are most likely to die due to sudden infant death syndrome.
Gross and his research team realized that by inducing a gene mutation into mice it would be possible to control their responses to serotonin. During the experiment, the researchers showed that baby mice died of cot death roughly at the same age and under similar circumstances as human children do.
"Those are pretty exciting findings," says Eugene Nattie, of Dartmouth University, who did not participate in the study.
The fact is that this is the first time serotonin is suspected to be a cot death triggering factor, since in 2006 a study revealed that serotonin can determine chemical changes in the brain, which in turn control automatic body functions.
The mutation induced by the research team was activated through an antibiotic and allowed them to make mice up to 20 percent less sensitive to serotonin. This was immediately corroborated to the fact that baby mice died in a relatively short amount of time after their birth. For example, up to 90 percent of all 40-day-old mice died after the mutation was activated, while 60-day-old mice experienced a fatality of only 30 percent.
Additionally, the mutant mice appeared to have some of the symptoms of human SIDS. In some cases their heart rate would slow enough to cause a several degree drop in body temperature, after which the heart rate would go back to normal again, rising the dangerously low temperature. This usually took place after REM sleep, when the body becomes even less sensitive to serotonin, which results in the brain losing control over the automatic body functions.
For now, the discovery brings little, but precious scientific insight into this horrible syndrome, but further study on mice should unravel some of the secrets behind similar processes taking place inside the human brain.
"We are actively searching, and this paper will stimulate people to actively search for markers that could be used in a test," says Nattie.