Summary: Researchers have confirmed previous findings linking abnormalities in serotonin to sudden death in infants. It is hoped the findings will help other researchers to develop biomarkers to identify infants at increased risk of SIDS.
Source: University of Adelaide.
University of Adelaide researchers have confirmed that abnormalities in a common brain chemical are linked to sudden infant death syndrome (SIDS).
In the first study of its kind looking at babies outside the United States, researchers from the University of Adelaide’s Adelaide Medical School investigated 41 cases of SIDS deaths and discovered striking abnormalities in chemical serotonin within the brain.
Serotonin, otherwise known as 5-HT, is a neurotransmitter found in different parts of the human body, including the central nervous system. Among its many roles, serotonin is involved in the regulation of sleep, and also control of the cardiovascular and respiratory systems.
This latest research, published in the Journal of Neuropathology & Experimental Neurology, confirms and supports the concept that brainstem dysfunction, resulting in significantly altered serotonin expression, is associated with some SIDS deaths.
SIDS is the sudden unexpected death of an infant under one year of age that cannot be explained after a thorough investigation, including an autopsy. It is the leading cause of death in infants between one month and one year of age in Australia and the developed world.
The research was conducted by PhD student Dr Fiona Bright under the supervision of University of Adelaide Professor of Pathology Roger Byard. Dr Bright today graduated with her PhD from the University of Adelaide.
Her work builds on research conducted in the United States at the Boston Children’s Hospital and Harvard Medical School, where Dr Bright was based for 18 months during her combined studies.
“Our research is significant because it has confirmed that abnormalities in serotonin in the brain are most definitely linked to cases of SIDS. This helps to support the findings of the American research,” Dr Bright says.
“Serotonin is a key neurochemical that plays an important role in the control and management of the complex respiratory, cardiovascular and autonomic systems within the human infant brainstem.
“Our research suggests that alterations in these neurochemicals may contribute to brainstem dysfunction during a critical postnatal developmental period. As a result, this could lead to an inability of a SIDS infant to appropriately respond to life-threatening events, such as lack of oxygen supply during sleep.
“Notably, the SIDS cases we studied were all linked to at least one major risk factor for SIDS, with more than half of the infants found in an adverse sleeping position and having had an illness one month prior to death,” Dr Bright says.
Professor Byard says: “Better understanding of the complex role of these neurochemicals, and the exact causes of their dysfunction in the brain, will help future research to develop potential biomarkers for infants at increased risk of SIDS.
“Ultimately, we hope that this work will lead to improved prevention strategies, helping to save baby’s lives and the emotional trauma experienced by many families.”
Funding: This research was funded under a Fellowship established by the River’s Gift SIDS charity.
“River’s Gift’s primary objective is to fund world-leading SIDS research to make a tangible contribution to the discovery of a cure for this heart-breaking loss of life,” says River’s Gift General Manager Karl Waddell.
“The University of Adelaide research is a significant step towards achieving that objective.”
Source: Fiona Bright – University of Adelaide
Image Source: NeuroscienceNews.com image is credited to Allan Korup.
Original Research: Abstract for “Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome” by Fiona M. Bright, PhD; Roger W. Byard, MD; Robert Vink, PhD; and David S. Paterson, PhD in Journal of Neuropathology & Experimental Neurology. Published online Apugust 1 2017 doi:10.1093/jnen/nlx071
Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome
Serotonin (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to key autonomic and respiratory nuclei in the brainstem and spinal cord regulating critical homeostatic functions. Multiple abnormalities in markers of 5-HT function in the medulla in sudden infant death syndrome (SIDS) have been reported, informing the hypothesis that at least a subset of SIDS cases is caused by deficits in 5-HT function resulting in impaired homeostatic responses to potentially life-threatening events during sleep. To investigate medullary 5-HT defects in SIDS further, we undertook qualitative analysis immunohistochemical assessment of 5-HT neuron expression within the medulla of SIDS infants (n41) and nonSIDS controls (n = 28) in an independent cohort from Forensic Science South Australia. Compared with controls SIDS cases had significantly higher 5-HT neuron numbers and density in addition to significantly altered 5-HT neuron morphology. Thus, for the first time, we replicated and corroborated previous observations of a significant abnormality in medullary 5-HT neuron expression in SIDS in a separate independent SIDS cohort. This study further supports the hypothesis that medullary 5-HT defects contribute to the pathogenesis of a subset of SIDS victims and provides additional evidence of a more complex abnormality in 5-HT neuron dysfunction specifically within the different caudal and rostral medullary 5-HT domains.
“Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome” by Fiona M. Bright, PhD; Roger W. Byard, MD; Robert Vink, PhD; and David S. Paterson, PhD in Journal of Neuropathology & Experimental Neurology. Published online Apugust 1 2017 doi:10.1093/jnen/nlx071