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July 01, 1996; 47 (1) Article

The apolipoprotein E epsilon 4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant

J. M. Olichney, L. A. Hansen, D. Galasko, T. Saitoh, C. R. Hofstetter, R. Katzman, L. J. Thal
First published July 1, 1996, DOI: https://doi.org/10.1212/WNL.47.1.190
J. M. Olichney
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L. A. Hansen
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D. Galasko
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T. Saitoh
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C. R. Hofstetter
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R. Katzman
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L. J. Thal
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Citation
The apolipoprotein E epsilon 4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant
J. M. Olichney, L. A. Hansen, D. Galasko, T. Saitoh, C. R. Hofstetter, R. Katzman, L. J. Thal
Neurology Jul 1996, 47 (1) 190-196; DOI: 10.1212/WNL.47.1.190

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Abstract

Objective: To determine the relationship between apolipoprotein E (apoE) genotype and neuropathologic lesions in Alzheimer's disease (AD) and Lewy body variant (LBV). Design: Retrospective genetic-neuropathologic study of AD and LBV cases. The main neuropathologic outcome measures were modeled as a function of apoE genotype, neuropathologic diagnosis, and gender. Age at death and duration of symptom effects were controlled for by ANCOVA. Patients: One hundred twenty-seven cases with neuropathologically diagnosed AD (n = 84) or LBV (n = 43). Main outcome measures: Quantitative scores of neuritic plaques (NPs), neurofibrillary tangles (NFTs), cerebral amyloid angiopathy (CAA) severity, and CAA prevalence were averaged across four brain regions: midfrontal, inferior parietal, superior temporal, and hippocampal. Results: The apoE epsilon 4 allele was associated with increased NPs within both AD and LBV. The epsilon 4 allele was associated with an increased frequency of CAA in the AD and LBV groups combined and in LBV alone. While CAA severity and NFTs were increased in the epsilon 4/4 homozygous cases when AD and LBV were combined, there were no significant effects within AD or LBV alone. Conclusions: The apoE epsilon 4 allele is strongly associated with increased NPs, but not neocortical NFTs, in both AD and LBV.

NEUROLOGY 1996;47: 190-196

  • Copyright 1996 by Advanstar Communications Inc.
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