Cited by 269Intracerebral and Subarachnoid Hemorrhage ResearchAlzheimer's disease research and treatmentsCerebrovascular and genetic disorders

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Association of apolipoprotein E ϵ2 and vasculopathy in cerebral amyloid angiopathy

Greenberg, S. M., Vonsattel, J.-P. G., Segal, A. Z., Chiu, R. I., Clatworthy, A. E., Liao, A., Hyman, B. T., Rebeck, G. W.·1998·Neurology

DOI 10.1212/wnl.50.4.961

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Abstract

Objective Hemorrhage related to cerebral amyloid angiopathy (CAA) appears to occur through a multistep pathway that includes deposition of beta-amyloid in cerebral vessels and specific vasculopathic changes in the amyloid-laden vessels, such as cracking of the vessel wall. Recent reports suggest a positive association between CAA-related hemorrhage and both the apolipoprotein E (APOE) epsilon4 allele and, unexpectedly, the APOE epsilon2 allele. Unlike APOE epsilon4, APOE epsilon2 does not appear to act through increased beta-amyloid deposition. We therefore sought to determine whether it might specifically accelerate the second step in this pathway, that is, development of the vasculopathic changes that lead to hemorrhage. Methods To determine the role of APOE in development of vasculopathic changes, we compared APOE genotypes in two groups of postmortem brains: 52 brains with complete amyloid replacement of vessel walls but without vasculopathic changes, and 23 brains with complete amyloid replacement of vessels with the accompanying changes of cracking of the vessel wall and paravascular leaking of blood. Results Frequency of APOE epsilon2 was significantly greater in the group with vasculopathy (0.09) than the group without (0.01, p = 0.03). The groups did not differ in mean age or extent of neuritic plaques. Analysis of a clinical series of patients with CAA-related hemorrhage confirmed an overrepresentation of APOE epsilon2 as well as an association between this allele a…

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“The role of apolipoprotein E (APOE) gene in lobar SICH has been reported and replicated in multiple ethnicities [15–22], in which both the ε2 and ε4 alleles are implicated in the CAA-related vascular damage.”
Background
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Authors: Greenberg, S. M., Vonsattel, J.-P. G., Segal, A. Z., Chiu, R. I., Clatworthy, A. E., Liao, A., Hyman, B. T., & Rebeck, G. W.
Affiliations: Harvard University (US)
ORCID: Greenberg, S. M.
Segal, A. Z.
Clatworthy, A. E.
Hyman, B. T.
Rebeck, G. W.
Venue: Neurology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1998-04
Volume: 50
Issue: 4
Pages: 961-965
ISSN: 0028-3878 (ISSN-L)
1526-632X
DOI: 10.1212/wnl.50.4.961
OpenAlex: W2041396523
Cited by: 267
References: 23
Citations by year: 2026: 7 · 2025: 10 · 2024: 11 · 2023: 6 · 2022: 6 · 2021: 10 · 2020: 8 · 2019: 11 · 2018: 12 · 2017: 9 · 2016: 4 · 2015: 15 · 2014: 9 · 2013: 15 · 2012: 12
FWCI: 7.43
Type: journal article
Language: en
Open access: closed
Locations: Neurology (publishedVersion)
PubMed (publishedVersion)
Funders: Chinese Academy of Agricultural Sciences
National Institute on Aging (AG14473, AG 12406, AG00725)
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: cerebral amyloid angiopathy, APOE ε4, intracerebral hemorrhage, vasculopathy, amyloid-beta deposition, postmortem brain
MeSH terms: Age Factors, Aged, Aged, 80 and over, Amyloidosis, Apolipoproteins E, Cerebral Arteries, Cerebral Hemorrhage, Genotype, Humans, Middle Aged, Cohort Studies, Apolipoprotein E2

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Association of apolipoprotein E ϵ2 and vasculopathy in cerebral amyloid angiopathy

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