Evidence map›Paper›PMID 30090055›Full record

ArticleFrontiers in neuroscience2018

Clusterin Is Required for β-Amyloid Toxicity in Human iPSC-Derived Neurons.

Jacqueline P Robbins, Leo Perfect, Elena M Ribe, Marcello Maresca, Adrià Dangla-Valls, Evangeline M Foster, Richard Killick, Paulina Nowosiad, Matthew J Reid, Lucia Dutan Polit and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 54 citations in OpenAlex.

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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

17 authors at 4 institutions in 2 countries.

Jacqueline P RobbinsDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Leo PerfectDepartment of Basic and Clinical Neuroscience, King's College London, London, United Kingdom.
Elena M RibeDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Marcello MarescaTranslational Genomics, Discovery Sciences, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Adrià Dangla-VallsDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Evangeline M FosterDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Richard KillickDepartment of Old Age Psychiatry, King's College London, London, United Kingdom.
Paulina NowosiadDepartment of Basic and Clinical Neuroscience, King's College London, London, United Kingdom.
Matthew J ReidDepartment of Basic and Clinical Neuroscience, King's College London, London, United Kingdom.
Lucia Dutan PolitDepartment of Basic and Clinical Neuroscience, King's College London, London, United Kingdom.
Alejo J NevadoDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Daniel EbnerNuffield Department of Medicine, Target Discovery Institute, University of Oxford, Oxford, United Kingdom.
Mohammad Bohlooly-YTranslational Genomics, Discovery Sciences, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Gothenburg, Sweden.
Noel BuckleyDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
Menelas N PangalosInnovative Medicines and Early Development Biotech Unit, AstraZeneca, Cambridge, United Kingdom.
Jack PriceDepartment of Basic and Clinical Neuroscience, King's College London, London, United Kingdom.
Simon LovestoneDepartment of Psychiatry, University of Oxford, Oxford, United Kingdom.
University of Oxford · GBKing's College London · GBAstraZeneca (Sweden) · SEAstraZeneca (United Kingdom) · GB

Funding

Medical Research Council 1246016Medical Research Council MC_PC_17215
6 · The paper itself

Abstract

Our understanding of the molecular processes underlying Alzheimer's disease (AD) is still limited, hindering the development of effective treatments, and highlighting the need for human-specific models. Advances in identifying components of the amyloid cascade are progressing, including the role of the protein clusterin in mediating β-amyloid (Aβ) toxicity. Mutations in the clusterin gene (CLU), a major genetic AD risk factor, are known to have important roles in Aβ processing. Here we investigate how CLU mediates Aβ-driven neurodegeneration in human induced pluripotent stem cell (iPSC)-derived neurons. We generated a novel CLU-knockout iPSC line by CRISPR/Cas9-mediated gene editing to investigate Aβ-mediated neurodegeneration in cortical neurons differentiated from wild type and CLU knockout iPSCs. We measured response to Aβ using an imaging assay and measured changes in gene expression using qPCR and RNA sequencing. In wild type neurons imaging indicated that neuronal processes degenerate following treatment with Aβ

Indexed as

Alzheimer’s diseaseamyloidclusterinCRISPR/Casinduced pluripotent stem cellsneurodegeneration

Identifiers

PMID30090055
PMCPMC6068261
OpenAlexW2883129597

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.