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Eng-King Tan, MD; Justina Tong, BSc; Stephanie Fook-Chong, MSc; Yuen Yih, MD; Meng-Cheong Wong, MD; Ratnagopal Pavanni, MD; Yi Zhao, MD

Arch Neurol. 2007;64(7):1056-1058.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Gaucher disease (GD) is a recessive inherited glycolipid storage disorder caused by a deficiency of the lysosomal enzyme glucocerebrosidase (GBA).¹ Recent observation of an association between Parkinson disease (PD) and GBA gene mutations in Ashkenazi Jewish patients has generated considerable scientific interest.² However, data on this association in non–Ashkenazi Jewish populations is still limited.^3-4 Two recent studies in white patients with PD reported a negative or questionable association with GBA mutations.^3-4 The GBA L444P mutation appears to be the most common mutation among Chinese patients with GD in Taiwan.⁵ However, GD is extremely rare in our country. To our knowledge, there has not been a single reported case of GD in our population. Using a case-control methodology, we conducted a genetic screen of 2 common GBA mutations (L444P and . . . [Full Text of this Article]

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