Evidence map›Paper›PMID 33767334›Full record

ArticleCommunications biology2021

Distribution of microRNA profiles in pre-clinical and clinical forms of murine and human prion disease.

Lesley Cheng, Camelia Quek, Xia Li, Shayne A Bellingham, Laura J Ellett, Mitch Shambrook, Saima Zafar, Inga Zerr, Victoria A Lawson, Andrew F Hill

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 13 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 4 institutions in 4 countries.

Lesley ChengDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, Australia. l.cheng@latrobe.edu.au.
Camelia QuekDepartment of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Melbourne, VIC, Australia.
Xia LiDepartment of Mathematics and Statistics, La Trobe University, Bundoora, VIC, Australia.
Shayne A BellinghamDepartment of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Melbourne, VIC, Australia.
Laura J EllettDepartment of Pathology, The University of Melbourne, Melbourne, VIC, Australia.
Mitch ShambrookDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, Australia.
Saima ZafarDepartment of Neurology, University Medical Center Göttingen and German Center for Neurodegenerative Diseases, Göttingen, Germany.
Inga ZerrDepartment of Neurology, University Medical Center Göttingen and German Center for Neurodegenerative Diseases, Göttingen, Germany.
Victoria A LawsonDepartment of Pathology, The University of Melbourne, Melbourne, VIC, Australia.
Andrew F HillDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, Australia. andrew.hill@latrobe.edu.au.ORCID 0000-0001-5581-2354
The University of Melbourne · AUGerman Center for Neurodegenerative Diseases · DEBiotechnology Institute · USLa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prion diseases are distinguished by long pre-clinical incubation periods during which prions actively propagate in the brain and cause neurodegeneration. In the pre-clinical stage, we hypothesize that upon prion infection, transcriptional changes occur that can lead to early neurodegeneration. A longitudinal analysis of miRNAs in pre-clinical and clinical forms of murine prion disease demonstrated dynamic expression changes during disease progression in the affected thalamus region and serum. Serum samples at each timepoint were collected whereby extracellular vesicles (EVs) were isolated and used to identify blood-based biomarkers reflective of pathology in the brain. Differentially expressed EV miRNAs were validated in human clinical samples from patients with human sporadic Creutzfeldt-Jakob disease (sCJD), with the molecular subtype at codon 129 either methionine-methionine (MM, n = 14) or valine-valine (VV, n = 12) compared to controls (n = 20). EV miRNA biomarkers associated with prion infection predicted sCJD with an AUC of 0.800 (85% sensitivity and 66.7% specificity) in a second independent validation cohort (n = 26) of sCJD and control patients with MM or VV subtype. This study discovered clinically relevant miRNAs that benefit diagnostic development to detect prion-related diseases and therapeutic development to inhibit prion infectivity.

Indexed as

AgedAged, 80 and overAnimalsBiomarkersBrainCreutzfeldt-Jakob SyndromeFemaleHumansMaleMiceMice, Inbred BALB CMicroRNAsMiddle AgedPrion DiseasesBiomarkersMicroRNAs

Identifiers

PMID33767334
PMCPMC7994852
OpenAlexW3138890662

What OpenQuestion holds

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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.