| Sign In to gain access to subscriptions and/or personal tools. |
The Sudden Infant Death Syndrome (SIDS): A Neuro-Molecular HypothesisInstitute of Forensic Neuropsychiatry, University of Salzburg, Ignaz-Harrerstrasse 79, 5020 Salzburg, Austria, bernhard.mitterauer{at}sbg.ac.at
Department of Biochemistry, Biocentre, University of Basel, Klingelbergstrasse 70, CH-4056 Basel, Switzerland
Institute of Legal Medicine, University of Bern, Buhlstrasse 20, CH-3012 Bern, Switzerland Most of the children who die before age 1 in developed countries do so for unknown reasons, and these deaths are attributed to the sudden infant death syndrome (SIDS). Prospective cardiorespiratory monitoring of infants has revealed that SIDS victims have subtle differences in breathing and heartbeat patterns compared to controls. Because death must involve cardiorespiratory arrest, a straightforward explanation for SIDS is failure on the part of pacemaker neurons controlling the rhythmical processes of breathing or heartbeat. Genes coding for hyperpolarization-activated pacemaker cation channels have recently been isolated and are expressed in the heart and the brain. The authors propose that mutations in these genes and in other genes required for cardiorespiratory pacemaker activity will predispose an individual to SIDS during a window of vulnerability present in the first year of life. Furthermore, mutations in clock genes can alter a variety of rhythmical processes and may indirectly disturb cardiorespiratory function as well.
Key Words: SIDS • Hyperpolarization activated cation channel • Pacemaker • Mutations • Clock genes
The Neuroscientist, Vol. 6, No. 3,
154-158 (2000) This article has been cited by other articles:
| ||||||||||||||
 |
|
|
 |
Sign In to gain access to subscriptions and/or personal tools.
