Correspondence |

Analysis of the LRRK2 G2019S Mutation in Alzheimer Disease

Cyrus P. Zabetian, MD, MS; Chris J. Lauricella, BS; Debby W. Tsuang, MD, MSc; James B. Leverenz, MD; Gerard D. Schellenberg, PhD; Haydeh Payami, PhD
Arch Neurol. 2006;63(1):156-157. doi:10.1001/archneur.63.1.156.
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Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene result in typical late-onset Parkinson disease (PD).1,2 Yet the neuropathological heterogeneity observed in such patients (eg, nigral degeneration alone or in combination with tau pathology, diffuse Lewy bodies, brainstem Lewy bodies, or anterior horn cell loss) suggests that LRRK2 might be involved in the pathogenesis of several neurodegenerative diseases.1,2 The potential role of LRRK2 in Alzheimer disease (AD) is of particular interest because the gene resides within a region on chromosome 12 previously linked to late-onset AD.3 The aim of this study was to screen a large sample of patients with AD for the presence of the LRRK2 mutation most common in PD (G2019S).4

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