Evidence map›Paper›PMID 25799409›Full record

ArticlePloS one2015

Hook proteins: association with Alzheimer pathology and regulatory role of hook3 in amyloid beta generation.

Lydia Herrmann, Caspar Wiegmann, Annika Arsalan-Werner, Isabel Hilbrich, Carsten Jäger, Katharina Flach, Anne Suttkus, Ingolf Lachmann, Thomas Arendt, Max Holzer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 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

10 authors at 1 institution in 1 country.

Lydia HerrmannPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Caspar WiegmannPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Annika Arsalan-WernerPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Isabel HilbrichPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Carsten JägerPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Katharina FlachPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Anne SuttkusPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Ingolf LachmannAJ Roboscreen GmbH, Leipzig, Germany.
Thomas ArendtPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Max HolzerPaul Flechsig Institute of Brain Research, Department of Molecular and Cellular Mechanism of Neurodegeneration, University of Leipzig, Leipzig, Germany.
Leipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in intracellular transport are implicated in the pathogenesis of Alzheimer's disease (AD). Hook proteins are a family of cytoplasmic linker proteins that participate in endosomal transport. In this study we show that Hook1 and Hook3 are expressed in neurons while Hook2 is predominantly expressed in astrocytes. Furthermore, Hook proteins are associated with pathological hallmarks in AD; Hook1 and Hook3 are localized to tau aggregates and Hook2 to glial components within amyloid plaques. Additionally, the expression of Hook3 is reduced in AD. Modelling of Hook3 deficiency in cultured cells leads to slowing of endosomal transport and increases β-amyloid production. We propose that Hook3 plays a role in pathogenic events exacerbating AD.

Indexed as

Down-RegulationAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesCell LineEndosomesFemaleHeLa CellsHumansMaleMiceMicrotubule-Associated ProteinsMiddle AgedAmyloid beta-Peptideshook1 protein, humanHook2 protein, humanhook3 protein, humanMicrotubule-Associated Proteins

Identifiers

PMID25799409
PMCPMC4370497
OpenAlexW2056012419

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.