Apolipoprotein E alters the processing of the β-amyloid precursor protein in APPV717F transgenic mice
Abstract
We have recently reported a critical role for apolipoprotein E (apoE) in the process of amyloid deposition and neuritic plaque formation in APP(V717F) transgenic (Tg) mice, an animal model of Alzheimer's disease (AD). In the present study, we have investigated whether the presence or absence of apoE alters the processing of the amyloid precursor protein (APP) to various fragments, including the beta-amyloid peptides (Abeta). Here we show that, in contrast to APP(V717F) Tg mice expressing apoE, APP(V717F) Tg mice deficient in apoE develop anti-Abeta immunoreactive multifocal aggregates, which contain the beta-cleaved C-terminal fragments (beta-CTFs) of APP. Tg mice deficient in apoE also display altered levels of mature full-length APP, increased amounts of beta-CTFs, as well as elevated levels of Abeta(1-40) and Abeta(1-42) in an age- and region-dependent manner when compared to Tg mice expressing apoE. Taken together, these data support a role for apoE in APP processing in vivo.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In young PDAPP mice prior to the onset of Aβ deposition, the lack of apoE may actually increase soluble Aβ levels.
“Interestingly, it has been shown that in young PDAPP mice prior to the onset of Aβ deposition, that the lack of apoE may actually increases soluble Aβ levels, a finding that is consistent with cell culture data (Dodart et al., 2002; Fagan et al., 2002).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Dodart et al., 2002
Cites
Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition
Bales, K. R., Verina, T., Dodel, R. C., Du, Y., Altstiel, L., Bender, M., Hyslop, P., Johnstone, E. M., Little, S. P., Cummins, D. J., et al. (1997) · Nature Genetics · doi:10.1038/ng1197-263 · Cited by 830 · see citing works
Self-citationBiere, A. L., Ostaszewski, B., Zhao, H., Gillespie, S., Younkin, S. G., & Selkoe, D. J. (1995) · Neurobiology of Disease · doi:10.1006/nbdi.1995.0019 · Cited by 52 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
The role of apolipoprotein E in Alzheimer's disease
Kim, J., Basak, J. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.06.026 · Cited by 1,661 · see citing works
Uddin, M. S., Kabir, M. T., Al Mamun, A., Abdel-Daim, M. M., Barreto, G. E., & Ashraf, G. M. (2019) · Molecular Neurobiology · doi:10.1007/s12035-018-1237-z · Cited by 212 · see citing works
Kitazawa, M., Medeiros, R., & M. LaFerla, F. (2012) · Current Pharmaceutical Design · doi:10.2174/138161212799315786 · Cited by 178 · see citing works
Introducing Human <i>APOE</i> into A<i>β</i> Transgenic Mouse Models
Tai, L. M., Youmans, K. L., Jungbauer, L., Yu, C., & LaDu, M. J. (2011) · International Journal of Alzheimer’s Disease · doi:10.4061/2011/810981 · Cited by 52 · see citing works
ApoE mimetic peptide decreases Aβ production in vitro and in vivo
Minami, S. S., Cordova, A., Cirrito, J. R., Tesoriero, J. A., Babus, L. W., Davis, G. C., Dakshanamurthy, S., Turner, R. S., Pak, D. T., Rebeck, G. W., et al. (2010) · Molecular Neurodegeneration · doi:10.1186/1750-1326-5-16 · Cited by 34 · see citing works
- Authors
- Dodart, J.-C., Bales, K. R., Johnstone, E. M., Little, S. P., & Paul, S. M.
- Affiliations
- Eli Lilly (United States) (US)
- Corresponding author
- Dodart, Jean-Cosme
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2002-11
- Volume
- 955
- Issue
- 1-2
- Pages
- 191-199
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2022440769
- Cited by
- 30
- References
- 2
- Citations by year
- 2026: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2018: 1 · 2017: 1 · 2014: 4 · 2013: 2 · 2012: 4
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, amyloid precursor protein, APP processing, Alzheimer's disease, amyloid-beta, apolipoprotein E deficiency, amyloid deposition, neuritic plaques, Aβ(1-40), amyloid-beta 42
- MeSH terms
- Age Factors, Animals, Apolipoproteins E, Brain, Male, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, Phenylalanine, Protein Processing, Post-Translational, Valine, Amyloid beta-Protein Precursor, Mice
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 ›
Are you an author, or do you see a problem with this page? Request a review
