Evidence map›Paper›PMID 27248362›Full record

ArticleBrain pathology (Zurich, Switzerland)2017

Clusterin levels are increased in Alzheimer's disease and influence the regional distribution of Aβ.

J Scott Miners, Polly Clarke, Seth Love

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  4. 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
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  13. Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  14. Pathways to Alzheimer's Disease: The Intersecting Roles of Clusterin and Apolipoprotein E in Amyloid-β Regulation and Neuronal Health.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
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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

3 authors at 2 institutions in 1 country.

J Scott MinersDementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, United Kingdom.
Polly ClarkeDementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, United Kingdom.
Seth LoveDementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, United Kingdom.
University of Bristol · GBUK Dementia Research Institute · GB

Funding

Medical Research Council MC_PC_14095
6 · The paper itself

Abstract

Clusterin, also known as apoJ, is a lipoprotein abundantly expressed within the CNS. It regulates Aβ fibril formation and toxicity and facilitates amyloid-β (Aβ) transport across the blood-brain barrier. Genome-wide association studies have shown variations in the clusterin gene (CLU) to influence the risk of developing sporadic Alzheimer's disease (AD). To explore whether clusterin modulates the regional deposition of Aβ, we measured levels of soluble (NP40-extracted) and insoluble (guanidine-HCl-extracted) clusterin, Aβ40 and Aβ42 by sandwich ELISA in brain regions with a predilection for amyloid pathology-mid-frontal cortex (MF), cingulate cortex (CC), parahippocampal cortex (PH), and regions with little or no pathology-thalamus (TH) and white matter (WM). Clusterin level was highest in regions with plaque pathology (MF, CC, PH and PC), approximately mirroring the regional distribution of Aβ. It was significantly higher in AD than controls, and correlated positively with Aβ42 and insoluble Aβ40. Soluble clusterin level rose significantly with severity of cerebral amyloid angiopathy, and in MF and PC regions was highest in APOE ɛ4 homozygotes. In the TH and WM (areas with little amyloid pathology) clusterin was unaltered in AD and did not correlate with Aβ level. There was a significant positive correlation between the concentration of clusterin and the regional levels of insoluble Aβ42; however, the molar ratio of clusterin : Aβ42 declined with insoluble Aβ42 level in a region-dependent manner, being lowest in regions with predilection for Aβ plaque pathology. Under physiological conditions, clusterin reduces aggregation and promotes clearance of Aβ. Our findings indicate that in AD, clusterin increases, particularly in regions with most abundant Aβ, but because the increase does not match the rising level of Aβ42, the molar ratio of clusterin : Aβ42 in those regions falls, probably contributing to Aβ deposition within the tissue.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EBrainCerebral Amyloid AngiopathyClusterinEnzyme-Linked Immunosorbent AssayHumansPeptide FragmentsPlaque, AmyloidAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Apolipoproteins ECLU protein, humanClusterinPeptide FragmentsAlzheimer's diseaseamyloid-βamyloid-β clearanceapoJcerebral amyloid angiopathyclusterinplaque

Identifiers

PMID27248362
PMCPMC8029153
OpenAlexW2418421474

What OpenQuestion holds

Textmetadata
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.