ArticleGenetics in medicine : official journal of the American College of Medical Genetics2019
Noncardiac genetic predisposition in sudden infant death syndrome.
Article in Genetics in medicine : official journal of the American College of Medical Genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Known pathogenic gene variants and new candidates detected in sudden unexpected infant death using whole genome sequencing.American journal of medical genetics. Part A · 2024Article
- The impact of damaging epilepsy and cardiac genetic variant burden in sudden death in the young.Genome medicine · 2024Article
- White Matter Imaging Phenotypes Mediate the Negative Causality of Mitochondrial DNA Copy Number on Sleep Apnea: A Bidirectional Mendelian Randomization Study and Mediation Analysis.Nature and science of sleep · 2024Article
- Risk of Sudden Infant Death Syndrome Among Siblings of Children Who Died of Sudden Infant Death Syndrome in Denmark.JAMA network open · 2023Article
- Sudden Infant Death Syndrome: Beyond Risk Factors.Life (Basel, Switzerland) · 2021Review
- Sudden Unexpected Death and the Mammalian Dive Response: Catastrophic Failure of a Complex Tightly Coupled System.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
15 authors at 9 institutions in 6 countries.
Funding
Abstract
purposeSudden infant death syndrome (SIDS) is the commonest cause of sudden death of an infant; however, the genetic basis remains poorly understood. We aimed to identify noncardiac genes underpinning SIDS and determine their prevalence compared with ethnically matched controls.
methodsUsing exome sequencing we assessed the yield of ultrarare nonsynonymous variants (minor allele frequency [MAF] ≤0.00005, dominant model; MAF ≤0.01, recessive model) in 278 European SIDS cases (62% male; average age =2.7 ± 2 months) versus 973 European controls across 61 noncardiac SIDS-susceptibility genes. The variants were classified according to American College of Medical Genetics and Genomics criteria. Case-control, gene-collapsing analysis was performed in eight candidate biological pathways previously implicated in SIDS pathogenesis.
resultsOverall 43/278 SIDS cases harbored an ultrarare single-nucleotide variant compared with 114/973 controls (15.5 vs. 11.7%, p=0.10). Only 2/61 noncardiac genes were significantly overrepresented in cases compared with controls (ECE1, 3/278 [1%] vs. 1/973 [0.1%] p=0.036; SLC6A4, 2/278 [0.7%] vs. 1/973 [0.1%] p=0.049). There was no difference in yield of pathogenic or likely pathogenic variants between cases and controls (1/278 [0.36%] vs. 4/973 [0.41%]; p=1.0). Gene-collapsing analysis did not identify any specific biological pathways to be significantly associated with SIDS.
conclusionsA monogenic basis for SIDS amongst the previously implicated noncardiac genes and their encoded biological pathways is negligible.
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