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Apolipoprotein E and obstructive sleep apnea: evaluating whether a candidate gene explains a linkage peak
Emma K Larkin1, Sanjay R Patel, Susan Redline
1Department of Epidemiology and Biostatistics, Case Western Reserve University, 11400 Euclid Avenue, Ste. 260, Cleveland, OH 44106-6083, USA. emma.larkin@case.edu
Genetic Epidemiology
|December 24, 2005
Summary
Genetic studies suggest a susceptibility locus for obstructive sleep apnea near Apoliprotein E (ApoE). While ApoE E2 allele is linked to higher sleep apnea prevalence, ApoE itself is unlikely the causative gene.
Area of Science:
- Genetics
- Sleep Medicine
- Epidemiology
Background:
- Obstructive sleep apnea (OSA) is a common disorder with a significant genetic component.
- Apoliprotein E (ApoE) has been previously implicated as a potential susceptibility locus for OSA.
Purpose of the Study:
- To investigate the genetic epidemiology of sleep apnea.
- To further assess the role of the ApoE gene in the susceptibility to obstructive sleep apnea.
Main Methods:
- Fine-mapping linkage analysis using ten microsatellites near ApoE on chromosome 19.
- Genotyping of ApoE in a large cohort (n=1,211).
- Association analysis and regression models including ApoE genotype as a covariate.
Main Results:
- Linkage analysis identified marker AFM210yg9 (p=0.00034) near ApoE, strengthening previous findings.
- Inclusion of ApoE E2 allele as a covariate reduced the linkage signal by 18%, indicating ApoE is not the primary driver.
- Association analysis revealed a higher prevalence of sleep apnea in individuals with the ApoE E2 allele.
Conclusions:
- A disease susceptibility locus for obstructive sleep apnea exists in the chromosomal region of ApoE.
- Apoliprotein E itself is unlikely to be the causative gene for obstructive sleep apnea, despite its association with the E2 allele.