Association of polymorphisms in the Tau and Saitohin genes with Parkinson’s disease

• Published in: Journal of neurology, neurosurgery and psychiatry Vol. 75; no. 3; pp. 478 - 480
• Main Authors: Levecque, C, Elbaz, A, Clavel, J, Vidal, J S, Amouyel, P, Alpérovitch, A, Tzourio, C, Chartier-Harlin, M C
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd 01.03.2004; BMJ; BMJ Publishing Group LTD; BMJ Publishing Group; BMJ Group
• Subjects: Age; Aged; Biological and medical sciences; Case-Control Studies; Family medical history; Female; Genetic Predisposition to Disease; haplotype; Haplotypes; Humans; Life Sciences; Male; Medical sciences; Middle Aged; Neurology; Odds Ratio; Parents & parenting; Parkinson Disease; Parkinson Disease - genetics; Parkinson Disease - pathology; Parkinson's disease; Pesticides; Polymorphism; Polymorphism, Genetic; Saitohin gene; Santé publique et épidémiologie; Short Report; Tau gene; tau Proteins; tau Proteins - genetics; France; Nervous system diseases; Central nervous system disease; Parkinson disease; Degenerative disease; Cerebral disorder; Extrapyramidal syndrome; Polymorphism
• ISSN: 0022-3050; 1468-330X
• DOI: 10.1136/jnnp.2003.015750

Background: The Saitohin gene has recently been identified in intron 9 of the Tau gene. Because an association between Parkinson’s disease and Tau has been described, Saitohin represents a candidate gene for Parkinson’s disease. Objective: To test these two genes for their association with Parkinson’s disease in a large community based case–control study. Results: Cases (n = 208) were more often homozygotes for the Tau H1 haplotype than controls (n = 483; odds ratio (OR) = 1.71 (95% confidence interval, 1.20 to 2.43); p = 0.003), and the saitohin Q allele was in complete linkage disequilibrium with the H1 haplotype. This association was stronger among cases with Parkinson’s disease onset below 65 years (⩽65 years: OR = 2.52 (1.49 to 4.25); p<0.001) than among those with older onset (>65 years: OR = 1.20 (0.73 to 1.98); p<0.47). Conclusions: The data suggest that there is a functional polymorphism at this locus involved in Parkinson’s disease.