Cited by 210Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Apolipoprotein E and Alzheimer's disease: the influence of apolipoprotein E on amyloid-β and other amyloidogenic proteins

Open access
Huynh, Tien-Phat V., Davis, Albert A., Ulrich, Jason D., Holtzman, David M.·2017·Journal of Lipid Research

Abstract

as the most significant genetic risk factor for late-onset AD, which accounts for >99% of cases. The apoE protein is hypothesized to affect AD pathogenesis through a variety of mechanisms, from its effects on the blood-brain barrier, the innate immune system, and synaptic function to the accumulation of amyloid-β (Aβ). Here, we discuss the role of apoE on the biophysical properties and metabolism of the Aβ peptide, the principal component of amyloid plaques and cerebral amyloid angiopathy (CAA). CAA is characterized by the deposition of amyloid proteins (including Aβ) in the leptomeningeal medium and small arteries, which is found in most AD cases but sometimes occurs as an independent entity. Accumulation of these pathologies in the brain is one of the pathological hallmarks of AD. Beyond Aβ, we will extend the discussion to the potential role of apoE on other amyloidogenic proteins found in AD, and also a number of diverse neurodegenerative diseases.

Integrity signals

Registry

Crossref · 10.1194/jlr.r075481

Cites

206 of 206 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • APOE levels are increased in microglia and amyloid plaques in Cnp−/−;5×FAD mice.

    “Results of co-immunostaining experiments showed increased levels of APOE, a well-known factor in Aβ aggregation40, in microglia (Fig. 4g) and amyloid plaques in Cnp−/−;5×FAD mice (Fig. 4h).”

Cites

Flagged first, then by citations

3 of the 209 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Huynh, T.-P. V., Davis, A. A., Ulrich, J. D., & Holtzman, D. M.
Affiliations
Washington University in St. Louis (US)
Corresponding author
Holtzman, David M.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2017-05
Volume
58
Issue
5
Pages
824-836
ISSN
0022-2275 (ISSN-L)
OpenAlex
W2591809865
Cited by
210
References
209
Citations by year
2026: 13 · 2025: 20 · 2024: 21 · 2023: 29 · 2022: 22 · 2021: 19 · 2020: 23 · 2019: 32 · 2018: 22 · 2017: 9
FWCI
2.89
Type
journal article
Language
en
Update notices
erratum (2018-08-01)
Open access
Locations
  • Journal of Lipid Research (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Institutes of Health (NS090934, AG047644)
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, Alzheimer's disease, amyloid-beta, cerebral amyloid angiopathy, amyloid plaques, amyloidogenic proteins, late-onset Alzheimer's disease, blood-brain barrier, innate immunity, synaptic function, amyloid-beta metabolism, neurodegenerative diseases
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Humans, Risk Factors, Amyloid beta-Peptides

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