Evidence map›Paper›PMID 30872998›Full record

ReviewFrontiers in neuroscience2019

Clusterin in Alzheimer's Disease: Mechanisms, Genetics, and Lessons From Other Pathologies.

Evangeline M Foster, Adrià Dangla-Valls, Simon Lovestone, Elena M Ribe, Noel J Buckley

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 8 pooled it
18.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 8 syntheses or guidelines pooled it, 377 citations in OpenAlex.

  1. Pooled it
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  9. Trial
  10. Article
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  12. Review
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  14. A First-In-Class Antibody Enabling Detection of Altered Peripheral Non-Phosphorylated Clusterin With Translational Potential in Dementia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  15. Review
  16. Article
  17. Single-cell transcriptomic analysis reveals APOE genotype-dependent sex differences in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  18. Article
  19. Article
  20. Review

156 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Evangeline M FosterDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Adrià Dangla-VallsDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Simon LovestoneDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Elena M RibeDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Noel J BuckleyDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
University of Oxford · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Clusterin (CLU) or APOJ is a multifunctional glycoprotein that has been implicated in several physiological and pathological states, including Alzheimer's disease (AD). With a prominent extracellular chaperone function, additional roles have been discussed for clusterin, including lipid transport and immune modulation, and it is involved in pathways common to several diseases such as cell death and survival, oxidative stress, and proteotoxic stress. Although clusterin is normally a secreted protein, it has also been found intracellularly under certain stress conditions. Multiple hypotheses have been proposed regarding the origin of intracellular clusterin, including specific biogenic processes leading to alternative transcripts and protein isoforms, but these lines of research are incomplete and contradictory. Current consensus is that intracellular clusterin is most likely to have exited the secretory pathway at some point or to have re-entered the cell after secretion. Clusterin's relationship with amyloid beta (Aβ) has been of great interest to the AD field, including clusterin's apparent role in altering Aβ aggregation and/or clearance. Additionally, clusterin has been more recently identified as a mediator of Aβ toxicity, as evidenced by the neuroprotective effect of

Indexed as

amyloidcell deathDKK1neurodegenerationneuroprotectionoxidative stressWnt signaling

Identifiers

PMID30872998
PMCPMC6403191
OpenAlexW2920516237

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.