Cot death link to brain abnormalities

A study in the Journal of the American Medical Association has shown that cellular defects in the brainstem may be a risk factor for sudden infant death syndrome (SIDS).

Sleeping baby
Sleeping baby
These abnormalities mean that a baby is unable to process serotonin (5-HT) a neurotransmitter essential for homeostatic control.

Serotonergic (5-HT) neurons project extensively in to the brainstem which helps regulate homeostatic functions such as breathing and temperature control.

Previously, abnormalities in 5-HT receptor binding had been identified in infants dying from SIDS. The authors of this study, therefore, investigated cellular defects in the 5-HT pathways of the medulla in SIDS cases.

The study revealed that the brainstems of SIDS cases had more serotonergic neurons, but less 5-HT receptors.

It is hoped that the results will provide some further evidence towards understanding SIDS.

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