Evidence map›Paper›PMID 27975168›Full record

ArticleMolecular neurobiology2018

Molecular Alterations in the Cerebellum of Sporadic Creutzfeldt-Jakob Disease Subtypes with DJ-1 as a Key Regulator of Oxidative Stress.

Waqas Tahir, Saima Zafar, Franc Llorens, Amandeep Singh Arora, Katrin Thüne, Matthias Schmitz, Nadine Gotzmann, Niels Kruse, Brit Mollenhauer, Juan Maria Torres and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 16 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

13 authors at 6 institutions in 3 countries.

Waqas TahirDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Saima ZafarDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany. sz_awaan@yahoo.com.
Franc LlorensDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Amandeep Singh AroraDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Katrin ThüneDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Matthias SchmitzDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Nadine GotzmannDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
Niels KruseInstitute of Neuropathology, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, 37075, Goettingen, Germany.
Brit MollenhauerInstitute of Neuropathology, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, 37075, Goettingen, Germany.
Juan Maria TorresInstituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Carretera de Algete a El Casar Km. 8,1 S/N, 28130, Valdeolmos, Madrid, Spain.
Olivier AndréolettiInstitut National de la Recherche Agronomique/Ecole Nationale Vétérinaire, Toulouse, France.
Isidre FerrerInstitute of Neuropathology, Hospitalet de Llobregat, IDIBELL-University Hospital Bellvitge, University of Barcelona, Barcelona, Spain.
Inga ZerrDepartment of Neurology, University Medical Center Goettingen (UMG) and German Center for Neurodegenerative Diseases (DZNE) Goettingen, Robert-Koch-Str., 40, 37075, Goettingen, Germany.
University of Göttingen · DEGerman Center for Neurodegenerative Diseases · DEUniversitätsmedizin Göttingen · DEInstitut d'Investigació Biomédica de Bellvitge · ESInstituto Nacional de Investigación y Tecnología Agraria y Alimentaria · ESInteraction Hôtes Agents Pathogènes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebellar damage and granular and Purkinje cell loss in sporadic Creutzfeldt-Jakob disease (sCJD) highlight a critical involvement of the cerebellum during symptomatic progression of the disease. In this project, global proteomic alterations in the cerebellum of brain from the two most prevalent subtypes (MM1 and VV2) of sCJD were studied. Two-dimensional gel electrophoresis (2DE) coupled mass spectrometric identification revealed 40 proteins in MM1 and 43 proteins in VV2 subtype to be differentially expressed. Of those, 12 proteins showed common differential expression in their expression between two subtypes. Differentially expressed proteins mainly belonged to (i) cell cycle, gene expression and cell death; (ii) cellular stress response/oxidative stress (OS) and (iii) signal transduction and synaptic functions, related molecular functions. We verified 10 differentially expressed proteins at transcriptional and translational level as well. Interestingly, protein deglycase DJ-1 (an antioxidative protein) showed an increase in its messenger RNA (mRNA) expression in both MM1 and VV2 subtypes but protein expression only in VV2 subtype in cerebellum of sCJD patients. Nuclear translocalization of DJ-1 confirmed its expressional alteration due to OS in sCJD. Downstream experiments showed the activation of nuclear factor erythroid-2 related factor 2 (Nrf2)/antioxidative response element (ARE) pathway. DJ-1 protein concentration was significantly increased during the clinical phase in cerebrospinal fluid of sCJD patients and also at presymptomatic and symptomatic stages in cerebellum of humanized PrP transgenic mice inoculated with sCJD (MM1 and VV2) brain. These results suggest the implication of oxidative stress during the pathophysiology of sCJD.

Indexed as

Oxidative StressAnimalsCerebellumCreutzfeldt-Jakob SyndromeDisease ProgressionHumansMice, KnockoutProtein Deglycase DJ-1ProteomicsReproducibility of ResultsRNA, MessengerSignal TransductionSoftwareTandem Mass SpectrometryPARK7 protein, humanPARK7 protein, mouseProtein Deglycase DJ-1RNA, MessengerAntioxidative response elementsMass spectrometryParkinson disease protein 7/protein deglycase DJ-1Sporadic Creutzfeldt–Jakob diseaseTwo-dimensional gel electrophoresis

Identifiers

PMID27975168
OpenAlexW2566647791

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.