Preprohypocretin polymorphisms in Parkinson disease patients reporting "sleep attacks".
OBJECTIVE
Previously, we found a significant association between the dopamine D2 receptor gene polymorphism Taq IA and sudden onset of sleep in patients with Parkinson disease. Here we evaluated the association between the preprohypocretin (-909T/C), (-22C/T), and (-20C/A) polymorphisms and sudden onset of sleep in the same population of patients with Parkinson disease.


METHODS
We conducted an association study analyzing the distribution of preprohypocretin polymorphisms in Germanic, caucasian Parkinson disease patients with and without sudden onset of sleep, matched according to drug therapy, disease duration, sex, and age.


METHODS
Movement disorders section at a university hospital.


METHODS
132 Parkinson disease patients with sudden onset of sleep and 132 Parkinson disease patients without sudden onset of sleep.


METHODS
Blood samples were taken from each participant and used for DNA extraction. Polymorphisms were analyzed by established polymerase chain reaction protocols or direct sequencing.


RESULTS
The variant allele T of the (-909T/C) preprohypocretin polymorphism was more commonly found in Parkinson disease patients with sudden onset of sleep. Statistical analysis showed that there were significant differences in the genotype (P = .024) and allele (P = .018) distribution between both groups. For heterozygous and homozygous carriers of allele T, the genotype relative-risk estimates for the presence of sudden onset of sleep were 2.01 (95% confidence interval: 0.76-5.34) and 2.81 (95% confidence interval: 1.09-7.25), respectively.


CONCLUSIONS
Our results show a significant association between the (-909T/C) preprohypocretin polymorphism and sudden onset of sleep in Parkinson disease. However, we could not demonstrate any interaction between the Taq IA and (-909T/C) polymorphisms with respect to the occurrence of sudden onset of sleep, suggesting that multiple genetic factors may contribute to the pathogenesis of this phenomenon.
Rissling
Ida
I
Department of Neurology, Philipps-University Marburg, Germany.
Körner
Yvonne
Y
Geller
Frank
F
Stiasny-Kolster
Karin
K
Oertel
Wolfgang H
WH
Möller
J Carsten
JC
D000483:Alleles; D012321:DNA-Directed RNA Polymerases; D006970:Disorders of Excessive Somnolence / Q000453:epidemiology*; D005260:Female; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D009479:Neuropeptides / Q000235:genetics*; D064446:Orexin Receptors; D000068797:Orexins; D010300:Parkinson Disease / Q000453:epidemiology* / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D017448:Receptors, Dopamine D2 / Q000235:genetics* / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D013378:Substantia Nigra / Q000378:metabolism; D011795:Surveys and Questionnaires; D017557:Ventral Tegmental Area / Q000378:metabolism
D047908:Intracellular Signaling Peptides and Proteins; D009479:Neuropeptides; D064446:Orexin Receptors; D000068797:Orexins; D017448:Receptors, Dopamine D2; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D012321:DNA-Directed RNA Polymerases; C455879:Taq sigma A