Announcement posted by Fenton Communications 03 Feb 2010
A new study has confirmed the link between serotonin abnormalities and Sudden Infant Death Syndrome (SIDS), bringing researchers a step closer to a cure for the fatal condition.
A new study has confirmed the link between serotonin abnormalities and Sudden Infant Death Syndrome (SIDS), bringing researchers a step closer to a cure for the fatal condition.
It is the first study to show that brainstem levels of serotonin and its biosynthetic enzyme are lower in infants who have died of SIDS, further indicating that SIDS is an abnormality of the function of the body.
The study, published today in the Journal of the American Medical Association, was led by Australian researcher Dr Jhodie Duncan from the Florey Neuroscience Institutes, with colleagues at the Children’s Hospital in Boston.
Dr Duncan said the research could lead to the development of a ‘biomarker’ to identify children with lower than normal serotonin and TPH2 levels, potentially leading to intervention strategies to prevent SIDS.
“Up to this point many researchers have grappled with whether serotonin production in SIDS infants was more, less or the same as in unaffected children,” said Dr Duncan.
“Our study has proven that in infants dying of SIDS there is lower TPH2 levels and reduced serotonin production and we believe that research models can now be developed that focus on increasing serotonin production and uptake.”
Dr Duncan conducted the study in Professor Hannah Kinney’s laboratory while on the exclusive NHMRC CJ Martin Fellowship to the United States.
“SIDS currently takes the life of 1 in every 2,000 infants. Massive national campaigns decades ago highlighted the risks associated with particular sleeping positions for infants under one year of age.
“Those initial campaigns worked to reduce SIDS related deaths substantially, but over the past decade the numbers have plateaued,” she said.
“We hope this research takes us a step closer to a cure.”
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It is the first study to show that brainstem levels of serotonin and its biosynthetic enzyme are lower in infants who have died of SIDS, further indicating that SIDS is an abnormality of the function of the body.
The study, published today in the Journal of the American Medical Association, was led by Australian researcher Dr Jhodie Duncan from the Florey Neuroscience Institutes, with colleagues at the Children’s Hospital in Boston.
Dr Duncan said the research could lead to the development of a ‘biomarker’ to identify children with lower than normal serotonin and TPH2 levels, potentially leading to intervention strategies to prevent SIDS.
“Up to this point many researchers have grappled with whether serotonin production in SIDS infants was more, less or the same as in unaffected children,” said Dr Duncan.
“Our study has proven that in infants dying of SIDS there is lower TPH2 levels and reduced serotonin production and we believe that research models can now be developed that focus on increasing serotonin production and uptake.”
Dr Duncan conducted the study in Professor Hannah Kinney’s laboratory while on the exclusive NHMRC CJ Martin Fellowship to the United States.
“SIDS currently takes the life of 1 in every 2,000 infants. Massive national campaigns decades ago highlighted the risks associated with particular sleeping positions for infants under one year of age.
“Those initial campaigns worked to reduce SIDS related deaths substantially, but over the past decade the numbers have plateaued,” she said.
“We hope this research takes us a step closer to a cure.”
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