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Human Apolipoprotein E2, E3, and E4 Isoform-Specific Transgenic Mice: Human-like Pattern of GlialandNeuronal Immunoreactivity in Central Nervous System Not Observed in Wild-Type Mice
Abstract
Apolipoprotein E (apoE) and its three major alleles (APOE2, E3, and E4) have been implicated in Alzheimer's disease and other neurological disorders. Little is known of the role apoE plays in normal brain function and pathology. To create a model to study apoE in brain, we have generated APOE transgenic mice using microinjection of allele-specific human genomic fragments to establish founders which were then bred to APOE knockout mice lacking a functional mouse apoE protein. This allows the study of apoE without interference from the endogenous mouse APOE gene. Results demonstrate that transgenic lines have been established that transcribe and express apoE appropriately in brain, liver, and other tissues. High cholesterol levels found in APOE knockout mice are substantially corrected in the APOE transgenic lines. ApoE immunoreactivity has been detected in glial cells and selected classes of neurons in all three isoform-specific transgenics. This pattern of immunoreactivity is similar to that observed in nonhuman primates and man, and contrasts with the strictly glial staining pattern of normal rodents.
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“These mice express ApoE via the endogenous promoter, and as a result, the turnover of ApoE should reflect the natural synthesis and clearance rates of the protein [22].”
From In Vivo Human Apolipoprotein E Isoform Fractional Turnover Rates in the CNS (2012) · cites this paper as [22]
In the citing paper
“However, under aging and stress conditions, neurons also produce apoE, albeit at lower levels than astrocytes [25, 26].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [26]
In the citing paper
“working model: Aging and/or stress induces neuronal expression of apoE.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [26]
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“ApoE2 mice were not used for this study, as they express apoE at levels much higher than the apoE3 or apoE4 mice (35); thus, it would have been impossible to determine whether any effects observed were due to the genotype or were simply occurring due to differences in expression levels of apoE.”
BackgroundMethodInfluentialBiological basis for amyloidogenesis in Alzheimer’S disease
Андреева, Т. В., Lukiw, W. J., & Rogaev, E. I. (2017) · Biochemistry (Moscow) · doi:10.1134/s0006297917020043 · Cited by 38
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BackgroundHuman apolipoprotein E allele-specific brain expressing transgenic mice
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Self-citationIdentification of Plasma Biomarkers of TBI Outcome Using Proteomic Approaches in an APOE Mouse Model
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Self-citationApolipoprotein E is found in astrocytes but not in microglia in the normal mouse brain
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“Human apoE3 and apoE4 transgenic mice were generated on an apoE-deficient C57BL/6J background, utilizing human apoE3 and apoE4 transgenic constructs as previously reported [24].”
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“Briefly, mice were obtained by microinjecting genomic sequences for human APOE3 or APOE4 into single-cell embryos from apoE-deficient mice.(21) Confirmation of the presence of human APOE and absence of endogenous mouse APOE gene was done by PCR as previously described.”
MethodSelf-citationGene action in the aging brain: an evolutionary biological perspective
MARTIN, G. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(01)00341-4 · Cited by 24
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Understanding the Human Condition: Experimental Strategies in Mammalian Genetics
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“In an additional, more simple experiment, it was necessary only to construct a transgenic mouse to study Alzheimer's disease because the human Apo E4 lipoprotein variant that influences Alzheimer's is a dominant allele (Xu et al. 1996).”
BackgroundOlfactory Evaluation in Alzheimer’s Disease Model Mice
Zhang, J., Zhao, Z., Sun, S., Li, J., Wang, Y., Dong, J., Yang, S. C., Lou, Y., Yang, J., Li, W., et al. (2022) · Brain Sciences · doi:10.3390/brainsci12050607 · Cited by 19
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Transgenic Models of Alzheimer's Disease
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“This work has been supported by grants from the NIA (AG15409) and the State of California (98-15717).”
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A Model Of Acute Subdural Hematoma In The Mouse
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“Transgenic mice have been created that express human apoE3 or apoE4 isoforms but lack endogenous murine apoE (Xu et al., 1996).”
Roses, A. D., Gilbert, J. R., Xu, P., Sullivan, P. M., Popko, B., Burkhart, D., Christian-Rothrock, T., Saunders, A. M., Maeda, N., & Schmechel, D. E. (1998) · Neurobiology of Aging · doi:10.1016/s0197-4580(98)00030-x · Cited by 19
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“Targeting the APOE ε4 gene in brains of patients with AD to express ApoE3 (or ApoE2) could prove beneficial and an attractive therapeutic possibility, which could be explored first in transgenic mice expressing human ApoE4 [94,95].”
Transplantation of neural stem cells modulates apolipoprotein E expression in a rat model of stroke
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“astrocytes [26,27], these mice probably best mimic the”
InfluentialRobertson, T. A., Dutton, N., Martins, R. N., Taddei, K., & Papadimitriou, J. M. (2000) · Neuroscience · doi:10.1016/s0306-4522(00)00126-3 · Cited by 15
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Self-citationAlteration of nitric oxide synthase activity in young and aged apolipoprotein E-deficient mice
Law, A. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00068-4 · Cited by 14
“Recent evidence shows hyperlipidemia, increased loss of synaptic terminals, and neuronal cytoskeleton abnormalities in the cortices and hippocampi of aged apoE-knockout animals [18,32,35].”
BackgroundWang, H., Zhang, L., Xia, Z., & Cui, J. Y. (2022) · Drug Metabolism and Disposition · doi:10.1124/dmd.121.000453 · Cited by 13
“…AD mouse model where the mouse ApoE gene was replaced with either the common allele (ApoE3) or the susceptible allele (ApoE4) of human origins (Xu et al., 1996; Bour et al., 2008) and investigated the molecular mechanisms underlying the pathogenesis of neurodegenerative diseases in vivo This…”
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Dolev, I., & Michaelson, D. M. (2006) · Journal of Alzheimer s Disease · doi:10.3233/jad-2006-102-313 · Cited by 13
Tagalakis, A. D., Dickson, J. G., Owen, J. S., & Simons, J. P. (2005) · Journal of Molecular Neuroscience · doi:10.1385/jmn:25:1:095 · Cited by 13
“Therefore, targeting the APOE4 gene in brains of patients with AD to express apoE3 (or apoE2) could prove beneficial, and an attractive therapeutic possibility, which could be explored first in transgenic mice expressing human apoE4 (Xu et al., 1996; Gong et al., 2002) 210,212.”
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Self-citationLoss of apolipoprotein E exacerbates the neonatal lethality of the Smith-Lemli-Opitz syndrome mouse
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“It is possible that mouse models that have been humanized with the APOE variants (APOE2, APOE3 or APOE4) may provide a better model to study the effects of APOE variations, as these express the variant APOEs and thus have lipoprotein kinetics significantly different than null mice [39,40].”
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“Mice Strains used for this study included C57BL/6J mice expressing human APOE2, APOE3 or APOE4 under the control of the endogenous murine APOE promoter, that have been previously validated (Xu et al., 1996; Sullivan et al., 1997).”
MethodEzra, Y., Oron, L., Moskovich, L., Roses, A. D., Beni, S. M., Shohami, E., & Michaelson, D. M. (2003) · Neuroscience · doi:10.1016/s0306-4522(03)00436-6 · Cited by 11
“Human apoE3 and apoE4 transgenic mice were generated on an apoE-deficient C57BL/6J background, utilizing human apoE3 and apoE4 transgenic constructs as previously reported (Xu et al., 1996).”
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APOE, Immune Factors, Sex, and Diet Interact to Shape Brain Networks in Mouse Models of Aging
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“In the CNS, both microglia and astrocytes synthesize and secrete apoE4 [13, 14].”
Adams, K. J., Wilson, J. G., Millington, D. S., Moseley, M. A., Colton, C. A., Thompson, J. W., & Gottschalk, W. K. (2021) · Journal of the American Society for Mass Spectrometry · doi:10.1021/jasms.1c00055 · Cited by 7
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“To model genetic risk for LOAD, we used mice lacking the mouse Apoe gene, and homozygous for the three major human APOE alleles [64, 65]: the high-risk gene APOE4, the control APOE3 and the protective APOE2 allele.”
MethodAPOE-Based Models of “Pre-Dementia”
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Metadata
- Authors
- Xu, P.-T., Schmechel, D., Rothrock-Christian, T., Burkhart, D. S., Qiu, H.-L., Popko, B., Sullivan, P., Maeda, N., Saunders, A. M., Roses, A. D., & Gilbert, J. R.
- Affiliations
- Duke University (US)
- University of North Carolina at Chapel Hill (US)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 1996-06
- Volume
- 3
- Issue
- 3
- Pages
- 229-245
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2081122171
- Cited by
- 178
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 6 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 2 · 2014: 2 · 2013: 4 · 2012: 6
- FWCI
- 7.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r35ag007922-07)
- National Institute on Aging (AG05 128, P50AG005128, AG07922)
- National Institute of Environmental Health Sciences (Y01-ES-40290)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- apolipoprotein E, APOE isoforms, APOE2, APOE3, APOE ε4, transgenic mice, ApoE-deficient mice, glial cells, neuronal expression, central nervous system, Alzheimer's disease, cholesterol levels
- MeSH terms
- Alleles, Animals, Apolipoproteins E, Central Nervous System, DNA, Humans, Mice, Transgenic, Neuroglia, Neurons, Reference Values, Transcription, Genetic, Protein Biosynthesis, Gene Library, Genome, Transgenes, Mice, Apolipoprotein E3, Apolipoprotein E4, Apolipoprotein E2
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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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