Murine versus human apolipoprotein E4: differential facilitation of and co-localization in cerebral amyloid angiopathy and amyloid plaques in APP transgenic mouse models
Open accessAbstract
INTRODUCTION: Amyloid β (Aβ) accumulates in the extracellular space as diffuse and neuritic plaques in Alzheimer's disease (AD). Aβ also deposits on the walls of arterioles as cerebral amyloid angiopathy (CAA) in most cases of AD and sometimes independently of AD. Apolipoprotein E (apoE) ɛ4 is associated with increases in both Aβ plaques and CAA in humans. Studies in mouse models that develop Aβ deposition have shown that murine apoE and human apoE4 have different abilities to facilitate plaque or CAA formation when studied independently. To better understand and compare the effects of murine apoE and human apoE4, we bred 5XFAD (line 7031) transgenic mice so that they expressed one copy of murine apoE and one copy of human apoE4 under the control of the normal murine apoE regulatory elements (5XFAD/apoE(m/4)). RESULTS: The 5XFAD/apoE(m/4) mice contained levels of parenchymal CAA that were intermediate between 5XFAD/apoE(m/m) and 5XFAD/apoE(4/4) mice. In 5XFAD/apoE(m/4) mice, we found that Aβ parenchymal plaques co-localized with much more apoE than did parenchymal CAA, suggesting differential co-aggregation of apoE with Aβ in plaques versus CAA. More importantly, within the brain parenchyma of the 5XFAD/apoE(m/4) mice, plaques contained more murine apoE, which on its own results in more pronounced and earlier plaque formation, while CAA contained more human apoE4 which on its own results in more pronounced CAA formation. We further confirmed the co-aggregation of mouse apoE with Aβ in plaques by showing a strong correlation between insoluble mouse apoE and insoluble Aβ in PS1APP-21/apoE(m/4) mice which develop plaques without CAA. CONCLUSIONS: These studies suggest that both murine apoE and human apoE4 facilitate differential opposing effects in influencing Aβ plaques versus CAA via different co-aggregation with these two amyloid lesions and set the stage for understanding these effects at a molecular level.
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In 5XFAD mice expressing one copy of murine ApoE and one copy of ApoE4, ApoE4 colocalized more with CAA while murine ApoE colocalized more with plaques.
“In 5XFAD mice that express one copy of murine ApoE and one copy of ApoE4, ApoE4 colocalized more with CAA while murine ApoE colocalized more with plaques [34].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [34]
The Results section reports that, in 5XFAD mice with one murine apoE and one apoE4 copy, plaques contained more murine apoE and parenchymal CAA contained more apoE4. The claim omits the parenchymal qualifier: the same section reports more murine apoE than apoE4 in leptomeningeal CAA. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe degree to which apoE colocalizes with amyloid β in plaques or CAA was associated with its ability to facilitate the corresponding lesions.
“The degree to which apoE colocalizes with amyloid β in plaques or CAA was associated with its ability to facilitate the corresponding lesions [34].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [34]
mAPOE has been shown to have different effects on Aβ plaque metabolism and formation compared to human APOE.
“However, mAPOE has been shown to have different effects on Aβ plaque metabolism and formation compared to human APOE [104, 105].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [105]
Expression of mouse ApoE resulted in greater plaque formation than expression of human ApoE, and mouse ApoE preferentially promoted the formation of parenchymal plaques, while human ApoE promoted the formation of CAA.
“Expression of mouse ApoE resulted in greater plaque formation than expression of human ApoE, and mouse ApoE preferentially promoted the formation of parenchymal plaques, while human ApoE promoted the formation of CAA [59, 60, 94].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [94]
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- Authors
- Liao, F., Zhang, T. J., Jiang, H., Lefton, K. B., Robinson, G. O., Vassar, R., Sullivan, P. M., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Northwestern University (US)
- Duke University (US)
- Corresponding author
- Holtzman, David M.
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2015-11-10
- Volume
- 3
- Issue
- 1
- Pages
- 70-70
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC4641345
- OpenAlex
- W2166531363
- Cited by
- 77
- References
- 43
- Citations by year
- 2026: 4 · 2025: 20 · 2024: 11 · 2023: 4 · 2022: 5 · 2021: 11 · 2020: 5 · 2019: 6 · 2018: 3 · 2017: 4 · 2016: 4
- FWCI
- 2.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- National Institutes of Health (S10 RR0227552)
- BrightFocus Foundation (A2013037F)
- National Institute on Aging (AG047644)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- APOE ε4, cerebral amyloid angiopathy, amyloid plaques, amyloid-beta, Alzheimer's disease, APP transgenic mice, 5xFAD mice, APOE isoforms, transgenic mouse model
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Brain, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Cerebral Amyloid Angiopathy, Mice, Presenilin-1, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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