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Glucocerebrosidase gene mutations and Parkinson disease in the Norwegian population

From the Department of Neuroscience (M.T.), Norwegian University of Science and Technology, Trondheim, Norway; Department of Neuroscience (M.T., O.A.R., M.J.F., L.P.), Mayo Clinic College of Medicine, Jacksonville, FL; and Department of Neurology (J.O.A.), St. Olav's Hospital, Trondheim, Norway.

Address correspondence and reprint requests to Dr. Mathias Toft, Department of Neuroscience, Norwegian University of Science and Technology, N-7489 Trondheim, Norway; e-mail: mathias.toft{at}ntnu.no

An association between mutations in the glucocerebrosidase (GBA) gene and Parkinson disease (PD) was recently reported in Ashkenazi Jews. The authors screened a series of 311 Norwegian patients with PD and 474 controls for 2 common functional mutations of the GBA protein, N370S and L444P. Seven patients (2.3%) and 8 controls (1.7%) carried a mutant GBA allele (p = 0.58). This study does not indicate increased susceptibility to PD in GBA mutations carriers in Norway.

The Udall Center at the Mayo Clinic Jacksonville (National Institute of Neurologic Disorders and Stroke P01 NS40256), the Research Council of Norway (153487/V50), Reberg's legacy, and the Unger-Vetlesen Medical Fund supported this study.

Disclosure: The authors report no conflicts of interest.

Received May 19, 2005. Accepted in final form October 24, 2005.

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