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Molecular Genetics of Sudden Infant Death Syndrome

  1. Cornelius Courts

Published Online: 15 APR 2013

DOI: 10.1002/9780470015902.a0022424

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eLS

How to Cite

Courts, C. 2013. Molecular Genetics of Sudden Infant Death Syndrome. eLS. .

Author Information

  1. University of Bonn, Bonn, Germany

Publication History

  1. Published Online: 15 APR 2013

Abstract

The sudden infant death syndrome (SIDS) is currently defined as the sudden unexpected death of an infant less than 1 year of age with onset of the fatal episode apparently occurring during sleep, which remains unexplained after a thorough investigation. SIDS, whose aetiology remains rather vague, is still the major cause of death among infants between 1 month and 1 year of age in industrialised countries with varying incidences in different subpopulations.

After touching on definitory approaches and several current hypotheses concerning SIDS aetiology, the triple risk hypothesis as an explanatory model for SIDS is introduced, followed by the discussion of associated genetic risk factors potentially contributing to or predisposing for the generation of a vulnerable infant that, when encountering an environmental trigger, may succumb to SIDS. An overview of current animal models for SIDS is presented and future prospects are briefly discussed.

Key Concepts:

  • A proper definition and strict adherence to diagnostic criteria is critical to valid SIDS research.

  • SIDS is multifactorial disease probably with a genetic predisposition.

  • The triple risk areas model is an explanatory approach that may be fitted to most hypotheses concerning SIDS aetiology.

  • Numerous and very different genetic variants are potentially predisposing for SIDS.

  • Current animal models for SIDS may be useful but can each only represent a subgroup of SIDS.

  • Functional studies of SIDS pathomechanisms are required.

Keywords:

  • sudden infant death syndrome;
  • triple risk model;
  • genetic predisposition;
  • brainstem hypothesis;
  • SIDS animal model