Possible Link between Lipid Metabolism and Cerebral Amyloid Angiopathy in Alzheimer’s Disease: A Role for High-Density Lipoproteins?
Abstract
Although apolipoprotein E4 (ApoE4) is a well-established risk factor for the development of Alzheimer's disease (AD), it is unclear how ApoE affects the progression of the disease. beta-amyloid (Abeta) is a major constituent of cerebrovascular amyloid deposits in brains of subjects with Alzheimer's disease. In cerebrospinal fluid and in plasma, Abeta is normally present in association with high density lipoproteins (HDL). These lipoproteins may play a role in the removal of excess cholesterol from the brain through interaction with ApoE and heparan sulphate proteoglycans (HSPG) in the subendothelial space of cerebral microvessels. At the same time, HDL may have a role in maintaining Abeta soluble and in mediating its clearance. Therefore, similar factors, e.g. HDL, ApoE and HSPG, may be involved in the regulation of reverse cholesterol transport in the brain and in the processing of Abeta. Alterations in the process of cholesterol secretion from the brain may contribute to the deposition of Abeta in the vascular wall.
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?
Innate immune function and brain cholesterol metabolism have a role in Alzheimer's disease.
“Ample evidence suggests a role for innate immune function and brain cholesterol metabolism in Alzheimer's disease (AD) (Mulder and Terwel, 1998;Heneka and O'Banion, 2007).”
From Critical Role of Astroglial Apolipoprotein E and Liver X Receptor-α Expression for Microglial Aβ Phagocytosis (2011) · cites this paper as Mulder and Terwel, 1998
Cites
Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Rimmler, J. B., Locke, P. A., Conneally, P. M., Schmader, K. E., et al. (1994) · Nature Genetics · doi:10.1038/ng0694-180 · Cited by 1,920 · see citing works
Ma, J., Yee, A., Brewer, H. B., Das, S., & Potter, H. (1994) · Nature · doi:10.1038/372092a0 · Cited by 871 · see citing works
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
Ellis, R. J., Olichney, J. M., Thal, L. J., Mirra, S. S., Morris, J. C., Beekly, D., & Heyman, A. (1996) · Neurology · doi:10.1212/wnl.46.6.1592 · Cited by 561 · see citing works
Nascent astrocyte particles differ from lipoproteins in CSF
LaDu, M. J., Gilligan, S. M., Lukens, J. R., Cabana, V. G., Reardon, C. A., Van Eldik, L. J., & Holtzman, D. M. (1998) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1998.70052070.x · Cited by 285 · see citing works
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 · Cited by 267 · see citing works
Ghersi‐Egea, J. ‐., Gorevic, P. D., Ghiso, J., Frangione, B., Patlak, C. S., & Fenstermacher, J. D. (1996) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1996.67020880.x · Cited by 222 · see citing works
Wisniewski, H. M., Wegiel, J., Wang, K. C., & Lach, B. (1992) · Acta Neuropathologica · doi:10.1007/bf00311383 · Cited by 221 · see citing works
Olichney, J. M., Hansen, L. A., Galasko, D., Saitoh, T., Hofstetter, C. R., Katzman, R., & Thal, L. J. (1996) · Neurology · doi:10.1212/wnl.47.1.190 · Cited by 216 · see citing works
Ji, Z.-S., Pitas, R. E., & Mahley, R. W. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.22.13452 · Cited by 134 · see citing works
DeMattos, R. B., Curtiss, L. K., & Williams, D. L. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.7.4206 · Cited by 123 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Han, X. (2005) · Current Alzheimer Research · doi:10.2174/1567205052772786 · Cited by 183 · see citing works
Terwel, D., Steffensen, K. R., Verghese, P. B., Kummer, M. P., Gustafsson, J.-Å., Holtzman, D. M., & Heneka, M. T. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.6546-10.2011 · Cited by 181 · see citing works
Self-citationMulder, M., Blokland, A., van den Berg, D.-J., Schulten, H., Bakker, A. H. F., Terwel, D., Honig, W., de Kloet, E. R., Havekes, L. M., Steinbusch, H. W. M., et al. (2001) · Laboratory Investigation · doi:10.1038/labinvest.3780307 · Cited by 74 · see citing works
Self-citationDifferential effects of apoE4 and activation of ABCA1 on brain and plasma lipoproteins
Boehm-Cagan, A., Bar, R., Harats, D., Shaish, A., Levkovitz, H., Bielicki, J. K., Johansson, J. O., & Michaelson, D. M. (2016) · PLOS ONE · doi:10.1371/journal.pone.0166195 · Cited by 29 · see citing works
- Authors
- Mulder, M., & Terwel, D.
- Affiliations
- Maastricht University (NL)
- Corresponding author
- Terwel, D.
- ORCID
- Venue
- Pathophysiology of Haemostasis and Thrombosis
- Publisher
- S. Karger AG
- Published
- 1998
- Volume
- 28
- Issue
- 3-4
- Pages
- 174-194
- ISSN
- 1424-8832 (ISSN-L)
- 1424-8840
- OpenAlex
- W2093997793
- Cited by
- 40
- References
- 11
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2021: 4 · 2020: 2 · 2019: 2 · 2017: 2 · 2016: 1 · 2015: 1 · 2012: 1
- FWCI
- 0.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pathophysiology of Haemostasis and Thrombosis (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- Alzheimer's disease, cerebral amyloid angiopathy, high-density lipoprotein, APOE ε4, amyloid-beta, heparan sulfate proteoglycans, reverse cholesterol transport, cholesterol secretion, amyloid-beta clearance, lipid metabolism, cerebral microvasculature
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Biological Transport, Cholesterol, Humans, Lipoproteins, HDL, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Heparan Sulfate Proteoglycans, Apolipoprotein E4
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
