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From the Departments of Neurology (Drs. Lippa, Smith, Swearer, Drachman, Pulaski-Salo, and Pollen) and Pathology (Drs. Lippa and Smith), University of Massachusetts Medical Center, Worcester, MA; Departments of Pathology (Dr. Ghetti), Medical and Molecular Genetics (Dr. Benson), Medicine (Dr. Benson), and Neurology (Dr. Farlow), Indiana University Medical Center, Indianapolis, IN; Veterans Affairs Richard L. Roudebush Medical Center (Dr. Benson), Indianapolis, IN; Department of Neurology (Dr. Nee), National Institutes of Health, Bethesda, MD; Department of Neurology (Dr. Hyman), Massachusetts General Hospital, Boston, MA; Department of Pathology (Dr. Robitaille), University of Montreal, Montreal, PQ, Canada; University of Toronto (Drs. Bergeron and St. George-Hyslop), Toronto, ON, Canada; Department of Neurology (Drs. Saunders and Roses), Duke University, Charleston, NC; Department of Pathology (Dr. Dickson), Albert Einstein College of Medicine, Bronx, NY; and Department of Pathology (Dr. Crain), Johns Hopkins University, Baltimore, MD.
Supported principally by NIA Grant AG-05134, and also by AG-10133, AG-70922, and AG-05128, the Alzheimer Association of Toronto, the Scottish Rite Charitable Foundation, the American Health Assistance Foundation, the Medical Research Council of Canada, and the National Institutes of Health.
Presented in part at the 46th annual meeting of the American Academy of Neurology, Washington, DC, May 1994.
Received May 4, 1995. Accepted in final form May 31, 1995.
Address correspondence and reprint requests to Dr. Carol F. Lippa, Department of Neurology, Room 556C, 9th Floor, Medical College of Pennsylvania and Hahnemann University, 3300 Henry Avenue, Philadelphia, PA 19004.
Whether all etiologic forms of Alzheimer's disease (AD) share a final common pathway is a major issue.We determined the severity and regional distribution of neuronal loss, amyloid plaques, neuritic plaques (NPs), and neurofibrillary tangles (NFTs), and calculated the ratio of neuronal loss to NPs and NFTs in brains of 19 familial AD (FAD) patients with linkage to chromosome 14, six AD patients with mutations of chromosome 21 (codon 717 of the beta-amyloid precursor protein gene), and 11 sporadic AD (SAD) patients. There was no difference in the pattern of distribution of the various pathologic features or in the ratio of neuronal loss to NPs or NFTs in any AD group. However, FAD groups could be distinguished from SAD by the greater severity and the lack of influence of apolipoprotein E genotype on pathology. These differences may reflect differences in age at onset rather than different etiopathologic mechanisms. The similarity of pathologic findings in the different AD groups provides evidence for a final common pathophysiologic pathway in AD.
NEUROLOGY 1996;46: 406-212
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