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Genotyping Sleep Disorders Patients

OBJECTIVE: The genetic susceptibility factors underlying sleep disorders might help us predict prognoses and responses to treatment. Several candidate polymorphisms for sleep disorders have been proposed, but there has as yet inadequate replication or validation that the candidates may be useful in...

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Autores principales: Kripke, Daniel F., Shadan, Farhad F., Dawson, Arthur, Cronin, John W., Jamil, Shazia M., Grizas, Alexandra P., Koziol, James A., Kline, Lawrence E.
Formato: Texto
Lenguaje:English
Publicado: Korean Neuropsychiatric Association 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848776/
https://www.ncbi.nlm.nih.gov/pubmed/20396431
http://dx.doi.org/10.4306/pi.2010.7.1.36
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author Kripke, Daniel F.
Shadan, Farhad F.
Dawson, Arthur
Cronin, John W.
Jamil, Shazia M.
Grizas, Alexandra P.
Koziol, James A.
Kline, Lawrence E.
author_facet Kripke, Daniel F.
Shadan, Farhad F.
Dawson, Arthur
Cronin, John W.
Jamil, Shazia M.
Grizas, Alexandra P.
Koziol, James A.
Kline, Lawrence E.
author_sort Kripke, Daniel F.
collection PubMed
description OBJECTIVE: The genetic susceptibility factors underlying sleep disorders might help us predict prognoses and responses to treatment. Several candidate polymorphisms for sleep disorders have been proposed, but there has as yet inadequate replication or validation that the candidates may be useful in the clinical setting. METHODS: To assess the validity of several candidate associations, we obtained saliva deoxyribonucleic acid (DNA) samples and clinical information from 360 consenting research participants who were undergoing clinical polysomnograms. Ten single nucleotide polymorphisms (SNPs) were genotyped. These were thought to be related to depression, circadian sleep disorders, sleep apnea, restless legs syndrome (RLS), excessive sleepiness, or to slow waves in sleep. RESULTS: With multivariate generalized linear models, the association of TEF rs738499 with depressive symptoms was confirmed. Equivocal statistical evidence of association of rs1801260 (the C3111T SNP in the CLOCK gene) with morningness/eveningness and an association of Apolipoprotein E (APOE) rs429358 with the Epworth Sleepiness Scale (ESS) were obtained, but these associations were not strong enough to be of clinical value by themselves. Predicted association of SNPs with sleep apnea, RLS, and slow wave sleep were not confirmed. CONCLUSION: The SNPs tested would not, by themselves, be of use for clinical genotyping in a sleep clinic.
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spelling pubmed-28487762010-04-14 Genotyping Sleep Disorders Patients Kripke, Daniel F. Shadan, Farhad F. Dawson, Arthur Cronin, John W. Jamil, Shazia M. Grizas, Alexandra P. Koziol, James A. Kline, Lawrence E. Psychiatry Investig Original Article OBJECTIVE: The genetic susceptibility factors underlying sleep disorders might help us predict prognoses and responses to treatment. Several candidate polymorphisms for sleep disorders have been proposed, but there has as yet inadequate replication or validation that the candidates may be useful in the clinical setting. METHODS: To assess the validity of several candidate associations, we obtained saliva deoxyribonucleic acid (DNA) samples and clinical information from 360 consenting research participants who were undergoing clinical polysomnograms. Ten single nucleotide polymorphisms (SNPs) were genotyped. These were thought to be related to depression, circadian sleep disorders, sleep apnea, restless legs syndrome (RLS), excessive sleepiness, or to slow waves in sleep. RESULTS: With multivariate generalized linear models, the association of TEF rs738499 with depressive symptoms was confirmed. Equivocal statistical evidence of association of rs1801260 (the C3111T SNP in the CLOCK gene) with morningness/eveningness and an association of Apolipoprotein E (APOE) rs429358 with the Epworth Sleepiness Scale (ESS) were obtained, but these associations were not strong enough to be of clinical value by themselves. Predicted association of SNPs with sleep apnea, RLS, and slow wave sleep were not confirmed. CONCLUSION: The SNPs tested would not, by themselves, be of use for clinical genotyping in a sleep clinic. Korean Neuropsychiatric Association 2010-03 2010-02-22 /pmc/articles/PMC2848776/ /pubmed/20396431 http://dx.doi.org/10.4306/pi.2010.7.1.36 Text en Copyright © 2010 Korean Neuropsychiatric Association http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kripke, Daniel F.
Shadan, Farhad F.
Dawson, Arthur
Cronin, John W.
Jamil, Shazia M.
Grizas, Alexandra P.
Koziol, James A.
Kline, Lawrence E.
Genotyping Sleep Disorders Patients
title Genotyping Sleep Disorders Patients
title_full Genotyping Sleep Disorders Patients
title_fullStr Genotyping Sleep Disorders Patients
title_full_unstemmed Genotyping Sleep Disorders Patients
title_short Genotyping Sleep Disorders Patients
title_sort genotyping sleep disorders patients
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848776/
https://www.ncbi.nlm.nih.gov/pubmed/20396431
http://dx.doi.org/10.4306/pi.2010.7.1.36
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