In a new attempt to explain the cause of SIDS (Sudden Infant
Death Syndrome) the researchers of the European Molecular Biology
Laboratory in Monterotondo,
Italy have
studied the effects of signalling molecule serotonin.
SIDS is the third leading cause of death among infants aged
between a week and a year, killing 2,500 infants yearly in the U.S.
and thousands more globally. Its causes are believed to be many and are
fiercely debated.
The Italian researchers have developed a mouse model of
SIDS, also known as cot or crib death.
According to their findings, an imbalance of the neuronal
signal serotonin in the brainstem is sufficient to cause sudden death in mice.
The brainstem is that part of the brain that ensures the
link with the spinal cord and the Italian researchers have based their theory on
the fact that victims of SIDS show alterations in those brainstem neurons that
communicate using the signalling molecule serotonin
They overexpressed an important receptor that regulates
serotonin signalling, called serotonin 1A autoreceptor.
"At first sight the mice were normal. But then they
suffered sporadic and unpredictable drops in heart rate and body temperature.
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," says Cornelius Gross, one of the researchers.
While a complete block of serotonin signalling does not lead
to death, upsetting its intricate balance by overexpressing serotonin 1A
autoreceptor can. In response to serotonin the receptor initiates a negative
feedback mechanism that reduces serotonin release and dampens down the signal
to the body.
The researchers caution, however, that it is unlikely that the
exact same molecular mechanism leads to SIDS in humans.
Nevertheless, the mouse
model will help to shed light on how serotonin signalling, when dysfunctional,
can be life-threatening.
In May this year, a new research coming from
British researchers has linked the bacterial infection with sudden infant death
syndrome (SIDS).
For the study, pediatricians from Great
Ormond Street
Hospital for Children in London reviewed autopsies
of 546 infants who had died of SIDS between 1996 and 2005. The researchers
found dangerous bacteria in 181 babies, or nearly half of the 365 whose deaths
could not be explained. Some 72 infant deaths had non-infective causes, such as
congenital heart disease or an accident.
The researchers found high levels of Staphylococcus aureus
and Escherichia coli bacterial in children who died of SIDS. Most of the
bacteria were detected in the babies’ lungs and spleens.
Last year a report of Bristol
University’s Institute of Child Life
and Health revealed that in case of nine out of ten cot deaths babies had
mothers who smoked during their pregnancy.
Before 1991, laying babies face down during their sleep had
been mainly the cause for SIDS. Since then, due to the Back to Sleep campaign,
which promoted parents should lay their babies on their backs to sleep, the
SIDS has dropped almost three quarters. In addition avoiding exposing your
child to cigarette smoke reduces this risk.