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*These authors contributed equally to this work.
From Neurogenetics (Drs. Morris, Houlden, and Wood), Dementia Research Group (Drs. Janssen and Rossor), and Neuropathology (Dr. Revesz), Institute of Neurology; Department of Neuropathology (Dr. Lantos and M. Khan), Institute of Psychiatry; and Reta Lila Weston Institute of Neurological Studies (Drs. Morris, Wood, and Lees), University College London, UK; Centre for Research in Neurodegenerative Diseases (Dr. Bergeron), Toronto, Ontario; and Kinsmen Laboratory of Neurological Research (Drs. Yasojima and McGeer), University of British Columbia, Vancouver, Canada; and Mayo Clinic Jacksonville (Drs. Hardy and Hutton, M. Baker), FL; Department of Pathology (Dr. Bigio), University of TexasSouthwestern Medical School, Dallas; and Department of Neurology (Dr. Grossman) and Center for Neurodegenerative Disease Research (Dr. Trojanowski) and Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, Philadelphia.
Address correspondence and reprint requests to Dr. Michael Hutton, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224.
Picks disease (PiD) is characterized by the deposition of tau protein as three-repeat tau Pick bodies, whereas progressive supranuclear palsy (PSP) involves the deposition of four-repeat tau neurofibrillary tangles. PSP is associated with the tau H1 haplotype. The authors investigated a possible association between PiD and the tau H1 or H2 haplotype. There was no difference between the tau H2 haplotype or H2H2 genotype frequency in PiD cases and control subjects. No tau mutations were identified in pathologically typical cases of PiD, with antibody 12-E8-negative Pick bodies.
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