Cited by 9Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Role of apolipoprotein E in β-amyloidogenesis: Isoform-specific effects on protofibril to fibril conversion of Aβ in vitro and brain Aβ deposition in vivo.

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Hori, Yukiko, Hashimoto, Tadafumi, Nomoto, Hidetoshi, Hyman, Bradley T., Iwatsubo, Takeshi·2018·Journal of Biological Chemistry

Abstract

VOLUME 290 (2015) PAGES 15163–15174 PAGE 15171: There was an error in the figure legend to Fig. 6. The second sentence of the legend should read as follows. “After co-incubation of the freshly solubilized Aβ with rec apoE2 (hatched column), rec apoE3 (gray column), rec apoE4 (black column), or without apoE (white column), Aβ protofibrils were isolated by SEC and further incubated for 24 and 48 h.” Additionally, under “Experimental procedures,” the first sentence of the “Protofibril Stability Assays” section should read as follows. “Freshly solubilized Aβ(1–42) peptides were coincubated with recombinant apoE2, apoE3, apoE4, or without apoE for 6 h and then Aβ protofibrils were isolated by SEC and further incubated for the indicated times.” This error does not affect the results or conclusions of this work.

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Crossref · 10.1074/jbc.aac118.003576

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  • The increased propensity of Aβ to oligomerize in the presence of APOE4 is considered a major mechanism by which APOE4 increases Alzheimer disease risk.

    “and the increased propensity of Aβ to oligomerize in the presence of APOE4 is considered a major mechanism by which APOE4 increases AD risk113–116 (Fig. 2c).”

    From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [114]

    Our indexed copy is an Additions and Corrections notice (p. 7267), not the original study's results. Its correction to the Fig. 6 legend describes incubating Aβ with apoE isoforms, but does not say whether APOE4 increases Aβ oligomerization or whether that is a major mechanism of Alzheimer disease risk. Searches for both points found no further relevant passage. (LLM, conf=0.74)

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Authors
Hori, Y., Hashimoto, T., Nomoto, H., Hyman, B. T., & Iwatsubo, T.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2018-05
Volume
293
Issue
19
Pages
7267
ISSN
0021-9258 (ISSN-L)
OpenAlex
W4239465682
Cited by
9
References
0
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2022: 1 · 2021: 2
FWCI
0.35
Type
journal article
Language
en
Open access
Locations
Journal of Biological Chemistry (publishedVersion, cc-by)
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-beta, amyloid protofibrils, APOE isoforms, APOE2, APOE3, APOE ε4, amyloid deposition, Alzheimer's disease

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