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From the Division of Neurology (A.R.), University of Saskatchewan and Saskatoon Health Region, Saskatoon, Saskatchewan, Canada; Department of Neuroscience (D.W.D., O.A.R., J.C.D., S.J.L., S.A.C., M.J.F.), Mayo Clinic College of Medicine, Jacksonville, Fl; Department of Pathology (C.A.R.), University of Saskatchewan and Saskatoon Health Region, Saskatoon, Saskatchewan, Canada; and Saskatchewan Center for Parkinson's Disease and Movement Disorders (C.A.R., M.L.R., M.J.F.), Royal University Hospital, Saskatoon, Saskatchewan, Canada.
Address correspondence and reprint requests to Dr. Matthew J. Farrer, Molecular Genetics Laboratory and Core, Morris K. Udall Parkinson's Disease Research Center of Excellence, Birdsall Building, Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224; e-mail: farrer.matthew{at}mayo.edu.
Lrrk2 G2019S is predominantly associated with 
-synuclein–immunopositive Lewy body pathology. We have identified Family SK where Lrrk2 G2019S segregates with slowly progressive parkinsonism and the affected proband has tau-immunopositive neurofibrillary tangle pathology. Thus -synucleinopathy and tauopathy, the predominant pathologies associated with parkinsonism, may be alternate outcomes of the same underlying genetic cause. Intriguingly, we observe no evidence of a direct interaction between either the tau or -synuclein protein with Lrrk2.
M.J.F. and D.W.D. are supported by NIA (P01 AG17216) and NIEHS (R01 ES013941). Mayo Clinic Jacksonville is a M.K. Udall PD Research Centre of Excellence (National Institute of Neurological Disorders and Stroke P50 NS40256).
Disclosure: The authors report no conflicts of interest.
Received November 21, 2005. Accepted in final form June 27, 2006.
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