Credit: alt_f4 /
Reads Mutations of a genetic material called Atoh1 could play a central role in sudden infant death syndrome, US researchers have found by studying in mice. The gene appears to be involved in the regulation of the respiratory reflex, which is believed to play a key role in sudden infant death syndrome. Atoh1 is active in a brain region that has been implicated in Sudden Infant Death Syndrome in another recent study. Presumably, the results from the studies on the mouse model can be transferred to humans, say the researchers to Wei-Hsiang Huang from Baylor College of Medicine in Houston. Sudden infant death is the most common cause of death in children beyond the neonatal period. In 2005, 323 babies died in Germany in this abrupt manner. A failure of the respiratory reflex has been considered a cause for some time. Normally, the brain triggers a kind of alarm when the carbon dioxide level in the blood rises abnormally, or the oxygen concentration drops. A kind of emergency signal then triggers intensified breaths and also serves as a wake-up stimulus. According to the current theories, this system fails in some infants, which is a deadly oxygen deficiency.

The researchers were able to show that neonatal animals died from a sudden infantile death if the genetic material Atoh1 was genetically engineered. About half of the mice died shortly after birth and the remainder showed persistent respiratory disorders. Further analysis by the researchers showed that the animals with Atoh1 had abnormal nerve structures in a brain area called retrotrapezoic nucleus, or RTN, which is networked to the respiratory center.

These are exactly the results of a recent study by Italian researchers: Anna Lavezzi from the University of Milan and her colleagues analyzed the brains of 58 infants who died of sudden childhood death. They found that 71 percent of the little ones had malformations in RTN. Further investigations should clarify the connections now further.

Wei-Hsiang Huang (Baylor College of Medicine, Houston) Neuron, doi: 10.1016 / j.neuron.2012.06.027 © Martin Vieweg advertisement


Recommended Editor'S Choice