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Neurology 1999;53:1415
© 1999 American Academy of Neurology
Articles

A study of five candidate genes in Parkinson’s disease and related neurodegenerative disorders

D. J. Nicholl, MRCP, PhD, P. Bennett, PhD, L. Hiller, BSc, V. Bonifati, MD, N. Vanacore, MD, G. Fabbrini, MD, R. Marconi, MD, C. Colosimo, MD, P. Lamberti, MD, F. Stocchi, MD, U. Bonuccelli, MD, P. Vieregge, MD, D. B. Ramsden, PhD, G. Meco, MD, A. C. Williams, MD and for the European Study Group on Atypical Parkinsonism

From the Departments of Clinical Neurology (Drs. Nicholl, Bennett, and Williams), Medicine (Dr. Ramsden) and Clinical Trials Unit (L. Hiller), Queen Elizabeth Hospital & Birmingham University, Birmingham, UK; the Department of Neurosciences (Drs. Bonifati, Colosimo, Fabbrini, Meco, Stocchi, and Vanacore), "La Sapienza" University, Rome, Italy; the Institute of Neurology (Dr. Lamberti), University of Bari, Italy; the Neurology Section (Dr. Marconi), "Misericordia" Hospital, Grosseto, Italy; the Department of Neuroscience, Section of Neurology (Dr. Bonucelli), University of Pisa, Italy; and the Department of Neurology (Dr. Vieregge), Medical University of Lubeck, Germany.

Address correspondence and reprint requests to Dr. David Nicholl, Department of Neurology, Queen Elizabeth Hospital, Birmingham, B15 2TH, UK; e-mail: d.j.nicholl{at}bham.ac.uk

OBJECTIVE: To determine whether reported genetic association of polymorphisms in the CYP2D6, CYP1A1, N-acetyltransferase 2 (NAT2), DAT1, and glutathione s-transferase M1 (GSTM1) genes with PD were evident in a population of 176 unrelated patients with sporadic PD and to extend these findings to other disease groups (familial PD [n = 30], ALS [n = 50], multiple system atrophy [n = 38], progressive supranuclear palsy [n = 35], and AD [n = 23]).

METHODS: A combination of allele-specific PCR and analysis of restriction fragment length polymorphisms were performed.

RESULTS: We genotyped 1,131 individuals. After matching each patient with a control subject by age, sex, ethnicity, and geographic origin, there was no association of any allele/genotype with any of the six disease groups. There was an increased frequency of NAT2 slow acetylators in the ALS group compared with controls (70% versus 50%; OR 2.33 [95% CI, 1.03 to 5.30]), but this was not significant after adjusting for multiple testing.

CONCLUSIONS: This is one of the most extensive candidate gene studies performed in PD and the first time that some of these loci have been studied in multiple system atrophy and progressive supranuclear palsy. In contrast with previous studies, we found no role for these polymorphisms in the etiology of PD, ALS, multiple system atrophy, progressive supranuclear palsy, or AD.

Key words: PD—Debrisoquine hydroxylase—N-acetyltransferase—Glutathione S-transferase—Dopamine transporter—Cytochrome P450.




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