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Genomic risk factors in sudden infant death syndrome

Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health efforts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-relate...

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Detalles Bibliográficos
Autores principales: Van Norstrand, David W, Ackerman, Michael J
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3016628/
https://www.ncbi.nlm.nih.gov/pubmed/21122164
http://dx.doi.org/10.1186/gm207
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author Van Norstrand, David W
Ackerman, Michael J
author_facet Van Norstrand, David W
Ackerman, Michael J
author_sort Van Norstrand, David W
collection PubMed
description Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health efforts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-related deaths have suggested genetic factors, and many studies have attempted to identify SIDS-associated genes. This has resulted in a large body of literature implicating various genes and their encoded proteins and signaling pathways in numerous cohorts of various sizes and ethnicities. This review has undertaken a systematic evaluation of these studies, identifying the pathways that have been implicated in these studies, including central nervous system pathways, cardiac channelopathies, immune dysfunction, metabolism/energy pathways, and nicotine response. This review also explores how new genomic techniques will aid in advancing our knowledge of the genomic risk factors associated with SIDS, including SNPs and copy number variation. Last, this review explores how the current information can be applied to aid in our assessment of the at risk infant population.
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spelling pubmed-30166282011-11-30 Genomic risk factors in sudden infant death syndrome Van Norstrand, David W Ackerman, Michael J Genome Med Review Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health efforts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-related deaths have suggested genetic factors, and many studies have attempted to identify SIDS-associated genes. This has resulted in a large body of literature implicating various genes and their encoded proteins and signaling pathways in numerous cohorts of various sizes and ethnicities. This review has undertaken a systematic evaluation of these studies, identifying the pathways that have been implicated in these studies, including central nervous system pathways, cardiac channelopathies, immune dysfunction, metabolism/energy pathways, and nicotine response. This review also explores how new genomic techniques will aid in advancing our knowledge of the genomic risk factors associated with SIDS, including SNPs and copy number variation. Last, this review explores how the current information can be applied to aid in our assessment of the at risk infant population. BioMed Central 2010-11-30 /pmc/articles/PMC3016628/ /pubmed/21122164 http://dx.doi.org/10.1186/gm207 Text en Copyright ©2010 BioMed Central Ltd
spellingShingle Review
Van Norstrand, David W
Ackerman, Michael J
Genomic risk factors in sudden infant death syndrome
title Genomic risk factors in sudden infant death syndrome
title_full Genomic risk factors in sudden infant death syndrome
title_fullStr Genomic risk factors in sudden infant death syndrome
title_full_unstemmed Genomic risk factors in sudden infant death syndrome
title_short Genomic risk factors in sudden infant death syndrome
title_sort genomic risk factors in sudden infant death syndrome
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3016628/
https://www.ncbi.nlm.nih.gov/pubmed/21122164
http://dx.doi.org/10.1186/gm207
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