Cited by 151Intracerebral and Subarachnoid Hemorrhage ResearchAlzheimer's disease research and treatmentsCerebrovascular and genetic disorders

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APOE-ε2 and APOE-ε4 Correlate With Increased Amyloid Accumulation in Cerebral Vasculature

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Nelson, Peter T., Pious, Nina M., Jicha, Gregory A., Wilcock, Donna M., Fardo, David W., Estus, Steven, Rebeck, G. William·2013·Journal of Neuropathology & Experimental Neurology

DOI 10.1097/nen.0b013e31829a25b9PMC PMC3715146

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Abstract

The APOE-ε4 allele correlates with increased risk of Alzheimer disease (AD) and increased parenchymal amyloid plaques. We tested how the APOE genotype correlated with cerebral amyloid angiopathy (CAA) by analyzing 371 brains for parenchymal and meningeal CAA in 4 brain regions (frontal, parietal, temporal, and occipital neocortex). The overall severity of CAA was highest in the occipital lobe. APOE-ε4/4 brains (n = 22) had the highest levels of CAA across regions. In the occipital lobe, nearly all APOE-ε4/4 cases were scored with the highest level of CAA (meninges, 95% of cases; parenchyma, 81%). In this brain region as in others, APOE-ε3/4 brains (n = 115) showed consistently less CAA than APOE-ε4/4 brains (meninges, 43%; parenchyma, 43%). APOE-ε3/3 brains (n = 182) showed even less CAA (meninges, 19%; parenchyma, 19%). Interestingly, APOE-ε2/3 cases (n = 42) had more CAA than APOE-ε3/3 (meninges, 44%; parenchyma, 32%), despite a reduced risk for AD in the APOE-ε2/3 individuals. APOE-ε4/4 brains also had the fewest regions without CAA, whereas APOE-ε3/3 brains had the most. Ordinal regression analyses demonstrated significant impacts of APOE-ε2 and APOE-ε4 on CAA at least in some brain regions. These data demonstrate that APOE genotype correlations with Aβ deposition in CAA only incompletely correspond to other AD-linked brain pathologies.

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Authors: Nelson, P. T., Pious, N. M., Jicha, G. A., Wilcock, D. M., Fardo, D. W., Estus, S., & Rebeck, G. W.
Affiliations: University of Kentucky (US)
Georgetown University (US)
Corresponding author: Rebeck, G. William
ORCID: Nelson, Peter T.
Jicha, Gregory A.
Wilcock, Donna M.
Fardo, David W.
Estus, Steven
Rebeck, G. William
Venue: Journal of Neuropathology & Experimental Neurology
Publisher: Oxford University Press (OUP)
Published: 2013-07
Volume: 72
Issue: 7
Pages: 708-715
ISSN: 0022-3069 (ISSN-L)
1554-6578
DOI: 10.1097/nen.0b013e31829a25b9
PMC: PMC3715146
OpenAlex: W2046985190
Cited by: 150
References: 43
Citations by year: 2026: 13 · 2025: 20 · 2024: 20 · 2023: 20 · 2022: 14 · 2021: 12 · 2020: 12 · 2019: 6 · 2018: 6 · 2017: 2 · 2016: 8 · 2015: 10 · 2014: 7
FWCI: 5.29
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Neuropathology & Experimental Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (P01AG030128, P30AG028383, R01AG035379)
Topics: Health Sciences › Medicine › Clinical Neurology › Intracerebral and Subarachnoid Hemorrhage Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Clinical Neurology › Cerebrovascular and genetic disorders
Keywords: APOE ε2, APOE ε4, APOE genotype, cerebral amyloid angiopathy, amyloid-beta deposition, Alzheimer's disease, occipital lobe, APOE ε3
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Blood Vessels, Cerebral Cortex, Female, Humans, Male, Logistic Models, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Apolipoprotein E4, Apolipoprotein E2

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APOE-ε2 and APOE-ε4 Correlate With Increased Amyloid Accumulation in Cerebral Vasculature

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