Evidence map›Paper›PMID 15897157›Full record

ArticleNeurotoxicity research2005

Association of apolipoprotein J-positive beta-amyloid plaques with dystrophic neurites in Alzheimer's disease brain.

M D Martin-Rehrmann, H-S Hoe, E M Capuani, G W Rebeck

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 40% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  14. Neuropathology of Alzheimer's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    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

4 authors at 3 institutions in 2 countries.

M D Martin-RehrmannAlzheimer Research Unit, 114 16th Street, Massachusetts General Hospital, Charlestown, MA 02129, USA.
H-S Hoe
E M Capuani
G W Rebeck
Georgetown University · USMassachusetts General Hospital · USUniversity of Tübingen · DE

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Functions of Lipoprotein Receptors in Alzheimer DiseaseR01AG014473 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI REBECK, G WILLIAM · 2002 to 2010
$2.7M
APOE AND ITS RECEPTORS IN NORMAL AND ALZHEIMERS BRAINR29AG014473 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI REBECK, G. WILLIAM · 1996 to 2000
$125k
NCHM CDC HHS HM31862NIA NIH HHS AG05134NIA NIH HHS AG14473
6 · The paper itself

Abstract

Apolipoprotein J (apoJ), also known as clusterin and SP-40,40, binds soluble beta-amyloid (Abeta and is up-regulated in the Alzheimer's disease (AD) brain. In the present study we classified apoJ-immunopositive Abeta deposits in AD temporal cortex, and found apoJ-immunoreactive plaques were often associated with dystrophic neurites. Quantitative immunohistochemical analysis of five AD brains showed that 29% of Abeta deposited in the parenchyma was associated with apoJ. Of Abeta deposits with apoJ immunopositivity, 71% were associated with phospho-tau-positive dystrophic neurites in the surrounding tissue. Conversely, 64% of phospho-tau-labeled neuritic deposits were labeled with apoJ. ApoJ was found at the core of these deposits, and co-localized with the amyloid staining agent thioflavine-S. To test the direct effects of apoJ on tau metabolism, we treated cells in culture with apoJ-containing conditioned media, and we injected apoJ-containing media into the rat hippocampus. Using both systems, we observed increases in levels of tau and phosphorylated tau. Our findings demonstrate that apoJ immunopositivity strongly correlates with the presence of amyloid and associated neuritic dystrophy in the neuropil of AD temporal cortex, and supports a model where extracellular apoJ facilitates the conversion of diffuse Abeta deposits into amyloid and enhances tau phosphorylation in neurites surrounding these of plaques.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalBlotting, WesternBrainBrain ChemistryCase-Control StudiesCell CountCells, CulturedClusterinFemaleGlycoproteinsHumansAmyloid beta-PeptidesAntibodies, MonoclonalCLU protein, humanClu protein, mouseClusterinGlycoproteinsMolecular Chaperonestau-1 monoclonal antibody

Identifiers

PMID15897157
OpenAlexW2086264330

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.