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Published online before print June 29, 2005, doi:10.1212/01.WNL.0000172630.22804.73)
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Received April 4, 2005
Accepted May 23, 2005

A clinic-based study of the LRRK2 gene in Parkinson disease yields new mutations

C. P. Zabetian MD, MS*, A. Samii MD, A. D. Mosley MD, MS, J. W. Roberts MD, B. C. Leis PhD, RN, D. Yearout BS, W. H. Raskind MD, PhD, and A. Griffith MD

From the Departments of Neurology (Drs. Zabetian and Samii and D. Yearout), Medicine (Dr. Raskind), and Psychiatry and Behavioral Sciences (Dr. Raskind), University of Washington School of Medicine, Seattle; Geriatric (Dr. Zabetian and D. Yearout), Northwest Parkinson’s Disease (Dr. Samii), and Mental Illness Research Education and Clinical Centers (Dr. Raskind), Veterans Affairs Puget Sound Health Care System, Seattle; Virginia Mason Medical Center (Dr. Roberts), Seattle; and Booth Gardner Parkinson’s Care Center (Drs. Mosley, Leis, and Griffith), Evergreen Hospital Medical Center, Kirkland, WA.


* To whom correspondence should be addressed. E-mail: zabetian{at}u.washington.edu.

Abstract-- Referral-based studies indicate that a mutation (G2019S) in exon 41 of the LRRK2 gene might be a common cause of Parkinson disease (PD). The authors sequenced leucine-rich repeat kinase 2 (LRRK2) exons 31, 35, and 41 in 371 consecutively recruited patients with PD and found mutations in six (1.6%) subjects, including two heterozygous for new putative pathogenic variants (R1441H, IVS31 + 3A->G). These data confirm the important contribution of LRRK2 to PD susceptibility in a clinic-based population.




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