Cited by 67Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Amyloid β-interacting partners in Alzheimer's disease: From accomplices to possible therapeutic targets

Han, Sun-Ho, Park, Jong-Chan, Mook-Jung, Inhee·2016·Progress in Neurobiology

Abstract

Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases in modern society because of insurmountable difficulties in early diagnosis and lack of therapeutic treatments. AD pathogenesis is tightly linked to the abnormal accumulation and aggregation of amyloid β (Aβ), seemingly the main causative factor of AD; however, intensive research on Aβ has not yet explained the complexity of AD pathogenesis. Consequently, the role of other supportive partners of Aβ have been elucidated and evaluated in the etiology of AD, and their potential molecular mechanisms have emerged as possible therapeutic targets. In this review, we compile information regarding Aβ-interacting partners in normal conditions and AD pathology, and analyze their etiological roles in diverse areas. Furthermore, we integrate this information into suggestions for probable clinical applications for AD diagnosis and therapeutics. We include Aβ-interacting partners localized to the cell surface and intracellular and extracellular compartments of different cell types ranging from the central nervous system to peripheral regions. Additionally, we expand the range of Aβ-interacting partners by including not only proteins, but also inorganic substances like metals, expecting that one of these partners may yield a critical breakthrough in the field of AD diagnostics and therapeutic drug development.

Integrity signals

Registry

Crossref · 10.1016/j.pneurobio.2015.12.004

Cites

351 of 351 references verified0 citation errors · 0 not checkable

Statistics

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

Claims the paper makes

This paper’s full text isn’t openly available, 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?

  • Overexpression of LRP minireceptor increased toxic amyloid β levels and caused deficits in learning and memory, whereas LDLR overexpression decreased amyloid β accumulation.

    “Overexpression of LRP minireceptor increased toxic amyloid β levels and caused the deficits in learning and memory, whereas LDLR overexpression decreased amyloid β accumulation [18].”

Cites

2 retracted

Flagged first, then by citations

4 of the 355 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Han, S.-H., Park, J.-C., & Mook-Jung, I.
Affiliations
Seoul National University (KR)
Venue
Progress in Neurobiology
Publisher
Elsevier BV
Published
2016-02
Volume
137
Pages
17-38
ISSN
0301-0082 (ISSN-L)
OpenAlex
W2207689373
Cited by
67
References
355
Citations by year
2026: 1 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 5 · 2019: 10 · 2018: 9 · 2017: 12 · 2016: 4
FWCI
1.02
Type
journal article
Language
en
Open access
closed
Locations
  • Progress in Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • NRF (2015R1A2A1A05001794, 2014M3C7A1046047, 2015M3C7A1028790, 2015R1C1A2A01053545)
  • MRC (2012R1A5A2A44671346)
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
Alzheimer's disease, amyloid-beta, protein-protein interaction, amyloid fibril formation, AD pathogenesis, therapeutic target
MeSH terms
Alzheimer Disease, Animals, Blood Proteins, Brain, Humans, Metals, Prions, Receptors, Cell Surface, Amyloid beta-Peptides, LDL-Receptor Related Proteins, 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