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The apolipoprotein E epsilon 4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant
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 groups combined and in and in LBV alone. While CAA severity and NETs were increased in the epsilon 4/4 homozygous case 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.
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“Rather, ApoE4 appears mainly to increase cerebrovascular amyloid burden, as previously reported, 33 as well as soluble amyloid burden.”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [33]
In the citing paper
“Collectively, then, our data do not confirm the suggestion that ApoE4 patients experience an increased neuritic amyloid plaque burden.33”
From Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease (1999) · cites this paper as [33]
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Metadata
- Authors
- Olichney, J. M., Hansen, L. A., Galasko, D., Saitoh, T., Hofstetter, C. R., Katzman, R., & Thal, L. J.
- Affiliations
- University of California San Diego (US)
- Venue
- Neurology
- Published
- 1996-07
- Volume
- 47
- Issue
- 1
- Pages
- 190-196
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W1966030100
- Cited by
- 216
- References
- 30
- Citations by year
- 2026: 5 · 2025: 1 · 2024: 10 · 2023: 1 · 2022: 6 · 2021: 4 · 2020: 11 · 2019: 4 · 2018: 4 · 2017: 2 · 2016: 3 · 2015: 10 · 2014: 8 · 2013: 5 · 2012: 6
- FWCI
- 4.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG05131, P50AG005131)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- APOE ε4, Alzheimer's disease, neuritic plaques, cerebral amyloid angiopathy, neurofibrillary tangles, genetic susceptibility, neuropathology
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Analysis of Variance, Apolipoproteins E, Female, Genotype, Humans, Male, Lewy Bodies, Cerebral Amyloid Angiopathy
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