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Familial and sporadic Alzheimer's disease: Neuropathology cannot exclude a final common pathway

Lippa, C. F., Saunders, A. M., Smith, T. W., Swearer, J. M., Drachman, D. A., Ghetti, B., Nee, L., Pulaski-Salo, D., Dickson, D., Robitaille, Y., Bergeron, C., Crain, B., Benson, M. D., Farlow, M., Hyman, B. T., St. George-Hyslop, P., Roses, A. D., Pollen, D. A.·1996·Neurology
DOI 10.1212/wnl.46.2.406
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Abstract

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 percursor 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.

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  • Familial Alzheimer's disease (FAD) accounts for fewer than 5% of AD cases; sporadic and familial forms share substantial phenotypic and molecular overlap, likely reflecting convergence on common pathogenic pathways.

    “Familial Alzheimer's disease (FAD) accounts for fewer than 5% of AD cases; however, sporadic and familial forms share substantial phenotypic and molecular overlap, likely reflecting convergence on common pathogenic pathways (Duara et al. 1993;Lippa et al. 1996).”

    From TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models (2026) · cites this paper as Lippa et al. 1996

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Metadata

Authors
Lippa, C. F., Saunders, A. M., Smith, T. W., Swearer, J. M., Drachman, D. A., Ghetti, B., Nee, L., Pulaski-Salo, D., Dickson, D., Robitaille, Y., Bergeron, C., Crain, B., Benson, M. D., Farlow, M., Hyman, B. T., St. George-Hyslop, P., Roses, A. D., & Pollen, D. A.
Venue
Neurology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1996-02
Volume
46
Issue
2
Pages
406-412
ISSN
  • 0028-3878
  • 1526-632X
DOI
10.1212/wnl.46.2.406
Cited by
97
References
4
Language
en

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