by Adam Spangler
July 10, 2008

By changing the control of the neurotransmitter serotonin in mice engineered to have abnormal brain chemistry, researchers may have stumbled upon the best model yet for sudden infant death syndrome (SIDS).

The July 2008 issue of the journal Nature reported that “the engineered mice showed symptoms that mirror human SIDS: sudden drops in heart rate and frequent deaths in early life. The majority of them died before reaching three months of age.”

The mice were meant for anxiety and aggression studies, but they immediately started dying. Scientists at the European Molecular Biology Laboratory in Monterotondo, Italy, eventually looked into the SIDS connection and determined that manipulating serotonin in a certain way could cause death.

How exactly the change in serotonin causes the symptoms is unknown. And unlike humans, the engineered mice die from symptoms after reaching adulthood. With humans, SIDS occurs only in infants and most often during napping, when serotonin levels fluctuate.

Further complicating the issue, a British study released in May 2008 in The Lancet found high levels of Staphylococcus aureus and Escherichia coli bacteria in children who had died of SIDS, suggesting a possible link, since most SIDS deaths occur between 8 and 10 weeks of age when the level of antibodies that protect babies from infection is low.

Determining whether or not the death of the mice is related directly to sleep is the next step for the Italian research team, with the immediate hope being that support for SIDS research will grow thanks to this serotonin link that puts scientists on track to unlocking this mysterious syndrome.