ApoER2 expression increases Aβ production while decreasing Amyloid Precursor Protein (APP) endocytosis: possible role in the partitioning of APP into lipid rafts and in the regulation of γ-secretase activity
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Background: The generation of the amyloid-β peptide (Aβ) through the proteolytic processing of the amyloid precursor protein (APP) is a central event in the pathogenesis of Alzheimer's disease (AD). Recent studies highlight APP endocytosis and localization to lipid rafts as important events favoring amyloidogenic processing. However, the precise mechanisms underlying these events are poorly understood. ApoER2 is a member of the low density lipoprotein receptor (LDL-R) family exhibiting slow endocytosis rate and a significant association with lipid rafts. Despite the important neurophysiological roles described for ApoER2, little is known regarding how ApoER2 regulates APP trafficking and processing. Results: Here, we demonstrate that ApoER2 physically interacts and co-localizes with APP. Remarkably, we found that ApoER2 increases cell surface APP levels and APP association with lipid rafts. The increase of cell surface APP requires the presence of ApoER2 cytoplasmic domain and is a result of decreased APP internalization rate. Unexpectedly, ApoER2 expression correlated with a significant increase in Aβ production and reduced levels of APP-CTFs. The increased Aβ production was dependent on the integrity of the NPxY endocytosis motif of ApoER2. We also found that expression of ApoER2 increased APP association with lipid rafts and increased γ-secretase activity, both of which might contribute to increased Aβ production. Conclusion: These findings show that ApoER2 negatively affects APP internalization. However, ApoER2 expression stimulates Aβ production by shifting the proportion of APP from the non-rafts to the raft membrane domains, thereby promoting β-secretase and γ-secretase mediated amyloidogenic processing and also by incrementing the activity of γ-secretase.
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Interactions of ApoER2 with APP affect APP processing, leading to increased production of Aβ.
“Interactions of ApoER2 with APP are known to affect APP processing, leading to the increased production of Aβ (Fuentealba et al., 2007; He et al., 2007).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Fuentealba et al., 2007
Co-expression of ApoER2 with APP promotes APP surface expression and lipid raft association of APP, both of which reduce Aβ formation.
“Co-expression of ApoER2 with APP promotes APP surface expression and the lipid raft association of APP, both of which reduce A formation (64).”
From Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses (2017) · cites this paper as [64]
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Bali, P. K., & Harris, W. R. (1990) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(90)90440-a · Cited by 46 · see citing works
Sun, X., & Soutar, A. K. (1999) · European Journal of Biochemistry · doi:10.1046/j.1432-1327.1999.00394.x · Cited by 44 · see citing works
Apolipoprotein E receptor 2 is involved in neuritic plaque formation in APP sw mice
Motoi, Y., Itaya, M., Mori, H., Mizuno, Y., Iwasaki, T., Hattori, H., Haga, S., & Ikeda, K. (2004) · Neuroscience Letters · doi:10.1016/j.neulet.2004.06.081 · Cited by 18 · see citing works
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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
Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease
Holtzman, D. M., Herz, J., & Bu, G. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006312 · Cited by 782 · see citing works
Self-citationAntisense oligonucleotides: translation from mouse models to human neurodegenerative diseases
Schoch, K. M., & Miller, T. M. (2017) · Neuron · doi:10.1016/j.neuron.2017.04.010 · Cited by 274 · see citing works
“…mediating AD pathogenesis is not fully understood, the receptor may modulate APP localization and processing, resulting in increased Ab production (Fuentealba et al., 2007; He et al., 2007), and its different splice variants confer its ligand binding and signaling function (Sun and Soutar, 1999).”
More than cholesterol transporters: lipoprotein receptors in CNS function and neurodegeneration
Lane-Donovan, C., Philips, G. T., & Herz, J. (2014) · Neuron · doi:10.1016/j.neuron.2014.08.005 · Cited by 158 · see citing works
Castellano, J. M., Deane, R., Gottesdiener, A. J., Verghese, P. B., Stewart, F. R., West, T., Paoletti, A. C., Kasper, T. R., DeMattos, R. B., Zlokovic, B. V., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1206446109 · Cited by 154 · see citing works
Marzolo, M.-P., & Bu, G. (2009) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2008.10.005 · Cited by 122 · see citing works
Self-citationReelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses
Wasser, C. R., & Herz, J. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.r116.766782 · Cited by 111 · see citing works
Functional Roles of the Interaction of APP and Lipoprotein Receptors
Pohlkamp, T., Wasser, C. R., & Herz, J. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00054 · Cited by 92 · see citing works
Sorting nexin 17 regulates ApoER2 recycling and reelin signaling
Sotelo, P., Farfán, P., Benitez, M. L., Bu, G., & Marzolo, M.-P. (2014) · PLoS ONE · doi:10.1371/journal.pone.0093672 · Cited by 47 · see citing works
Self-citationNeurotrophins regulate ApoER2 proteolysis through activation of the Trk signaling pathway
Larios, J. A., Jausoro, I., Benitez, M.-L., Bronfman, F. C., & Marzolo, M.-P. (2014) · BMC Neuroscience · doi:10.1186/1471-2202-15-108 · Cited by 12 · see citing works
Self-citation
- Authors
- Fuentealba, R. A., Barría, M. I., Lee, J., Cam, J., Araya, C., Escudero, C. A., Inestrosa, N. C., Bronfman, F. C., Bu, G., & Marzolo, M.-P.
- Affiliations
- Pontificia Universidad Católica de Chile (CL)
- Washington University in St. Louis (US)
- ORCID
- Venue
- Molecular Neurodegeneration
- Published
- 2007-07-09
- Volume
- 2
- Issue
- 1
- Pages
- 14-14
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC1939850
- OpenAlex
- W2137318731
- Cited by
- 70
- References
- 88
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 4 · 2017: 4 · 2016: 5 · 2015: 3 · 2014: 8 · 2013: 3 · 2012: 8
- FWCI
- 4.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Alzheimer's Association
- Washington University in St. Louis
- KU Leuven
- Universidad de Chile
- Instituto Millenium
- Pontificia Universidad Católica de Chile
- National Institute on Aging (R01AG027924)
- National Cancer Institute
- Fogarty International Center (R03TW006456)
- Fondo de Financiamiento de Centros de Investigación en Áreas Prioritarias (13980001)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- ApoER2, amyloid precursor protein, amyloid-beta production, APP endocytosis, lipid rafts, gamma-secretase, Alzheimer's disease, APP trafficking, NPXY motif, beta-secretase, LDL receptor family
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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