The apolipoprotein E ε4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant

John M Olichney, L. A. Hansen, D. Galasko, T. Saitoh, C. R. Hofstetter, R. Katzman, L. J. Thal

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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 ε4 allele was associated with increased NPs within both AD and LBV. The ε4 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 ε4/4 homozygous cases when AD and LBV were combined, there were no significant effects within AD or LBV alone. Conclusions: The apoE ε4 allele is strongly associated with increased NPs, but not neocortical NFTs, in both AD and LBV.

Original languageEnglish (US)
Pages (from-to)190-196
Number of pages7
JournalNeurology
Volume47
Issue number1
StatePublished - Jul 1996

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Cerebral Amyloid Angiopathy
Apolipoprotein E4
Amyloid Plaques
Alleles
Neurofibrillary Tangles
Lewy Bodies
Apolipoproteins E
Genotype
Outcome Assessment (Health Care)
Lewy Body Variant of Alzheimer Disease
Alzheimer Disease
Brain

ASJC Scopus subject areas

  • Neuroscience(all)

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The apolipoprotein E ε4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant. / Olichney, John M; Hansen, L. A.; Galasko, D.; Saitoh, T.; Hofstetter, C. R.; Katzman, R.; Thal, L. J.

In: Neurology, Vol. 47, No. 1, 07.1996, p. 190-196.

Research output: Contribution to journalArticle

Olichney, John M ; Hansen, L. A. ; Galasko, D. ; Saitoh, T. ; Hofstetter, C. R. ; Katzman, R. ; Thal, L. J. / The apolipoprotein E ε4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant. In: Neurology. 1996 ; Vol. 47, No. 1. pp. 190-196.
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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 ε4 allele was associated with increased NPs within both AD and LBV. The ε4 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 ε4/4 homozygous cases when AD and LBV were combined, there were no significant effects within AD or LBV alone. Conclusions: The apoE ε4 allele is strongly associated with increased NPs, but not neocortical NFTs, in both AD and LBV.",
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T1 - The apolipoprotein E ε4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant

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AU - Hansen, L. A.

AU - Galasko, D.

AU - Saitoh, T.

AU - Hofstetter, C. R.

AU - Katzman, R.

AU - Thal, L. J.

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N2 - 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 ε4 allele was associated with increased NPs within both AD and LBV. The ε4 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 ε4/4 homozygous cases when AD and LBV were combined, there were no significant effects within AD or LBV alone. Conclusions: The apoE ε4 allele is strongly associated with increased NPs, but not neocortical NFTs, in both AD and LBV.

AB - 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 ε4 allele was associated with increased NPs within both AD and LBV. The ε4 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 ε4/4 homozygous cases when AD and LBV were combined, there were no significant effects within AD or LBV alone. Conclusions: The apoE ε4 allele is strongly associated with increased NPs, but not neocortical NFTs, in both AD and LBV.

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