Evidence map›Paper›PMID 32678125›Full record

ArticleScientific reports2020

Prolongation of metallothionein induction combats Aß and α-synuclein toxicity in aged transgenic Caenorhabditis elegans.

Dagmar Pretsch, Judith Maria Rollinger, Axel Schmid, Miroslav Genov, Teresa Wöhrer, Liselotte Krenn, Mark Moloney, Ameya Kasture, Thomas Hummel, Alexander Pretsch

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Azepine-Indole Alkaloids FromFrontiers in neuroscience · 2022
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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 4 institutions in 2 countries.

Dagmar PretschOxford Antibiotic Group GmbH, Konrad-Lorenz-Straße 24, 3430, Tulln, Austria. d.pretsch@oxfordantibioticgroup.com.
Judith Maria RollingerDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
Axel SchmidDepartment of Neuroscience and Developmental Biology, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
Miroslav GenovOxford Antibiotic Group GmbH, Konrad-Lorenz-Straße 24, 3430, Tulln, Austria.ORCID http://orcid.org/0000-0001-6854-4387
Teresa WöhrerOxford Antibiotic Group GmbH, Konrad-Lorenz-Straße 24, 3430, Tulln, Austria.
Liselotte KrennDepartment of Pharmacognosy, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
Mark MoloneyDepartment of Chemistry, University of Oxford, 12 Mansfield Road, Oxford, OX1 3TA, UK.
Ameya KastureDepartment of Neuroscience and Developmental Biology, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
Thomas HummelDepartment of Neuroscience and Developmental Biology, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
Alexander PretschOxford Antibiotic Group GmbH, Konrad-Lorenz-Straße 24, 3430, Tulln, Austria.
University of Vienna · ATKonrad Lorenz Institute for Evolution and Cognition Research · ATAustrian Centre of Industrial Biotechnology (Austria) · ATUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative disorders (ND) like Alzheimer's (AD), Parkinson's (PD), Huntington's or Prion diseases share similar pathological features. They are all age dependent and are often associated with disruptions in analogous metabolic processes such as protein aggregation and oxidative stress, both of which involve metal ions like copper, manganese and iron. Bush and Tanzi proposed 2008 in the 'metal hypothesis of Alzheimer's disease' that a breakdown in metal homeostasis is the main cause of NDs, and drugs restoring metal homeostasis are promising novel therapeutic strategies. We report here that metallothionein (MT), an endogenous metal detoxifying protein, is increased in young amyloid ß (Aß) expressing Caenorhabditis elegans, whereas it is not in wild type strains. Further MT induction collapsed in 8 days old transgenic worms, indicating the age dependency of disease outbreak, and sharing intriguing parallels to diminished MT levels in human brains of AD. A medium throughput screening assay method was established to search for compounds increasing the MT level. Compounds known to induce MT release like progesterone, ZnSO

Indexed as

Agingalpha-SynucleinAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedBenzothiazolesCaenorhabditis elegansCaenorhabditis elegans ProteinsClioquinolDisease Models, AnimalEmodinGene Knockdown TechniquesHomeostasisMetallothioneinMetalsalpha-SynucleinAmyloid beta-PeptidesBenzothiazolesCaenorhabditis elegans ProteinsClioquinolEmodinMetallothioneinMetalsNeuroprotective AgentsQuercetinthioflavin T

Identifiers

PMID32678125
PMCPMC7366685
OpenAlexW3042427761

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.