Evidence map›Paper›PMID 29434051›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2018

Downregulation of exosomal miR-204-5p and miR-632 as a biomarker for FTD: a GENFI study.

Raphael Schneider, Paul McKeever, TaeHyung Kim, Caroline Graff, John Cornelis van Swieten, Anna Karydas, Adam Boxer, Howie Rosen, Bruce L Miller, Robert Laforce and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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  19. Evaluating the causal association between microRNAs and amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Article
  20. Frontotemporal lobar degeneration.Nature reviews. Disease primers · 2023
    Review
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

19 authors at 10 institutions in 7 countries.

Raphael SchneiderDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.ORCID 0000-0003-1776-2418
Paul McKeeverDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
TaeHyung KimDepartment of Computer Science, University of Toronto, Toronto, Ontario, Canada.
Caroline GraffDepartment of Neurobiology, Karolinska Institute, Stockholm, Sweden.
John Cornelis van SwietenDepartment of Neurology, Erasmus Medical Center, Rotterdam, The Netherlands.
Anna KarydasDepartment of Neurology, University of California, San Francisco, California, USA.
Adam BoxerDepartment of Neurology, University of California, San Francisco, California, USA.
Howie RosenDepartment of Neurology, University of California, San Francisco, California, USA.
Bruce L MillerDepartment of Neurology, University of California, San Francisco, California, USA.
Robert LaforceDépartement des Sciences Neurologiques, Université Laval, Quebec, Canada.
Daniela GalimbertiCentro Dino Ferrari, Fondazione Ca' Granda IRCCS Ospedale Policlinico, University of Milan, Milan, Italy.
Mario MasellisLC Campbell Cognitive Neurology Research Unit, University of Toronto, Toronto, Ontario, Canada.
Barbara BorroniNeurology Unit, Centre for Ageing Brain and Neurodegenerative Disorders, University of Brescia, Brescia, Italy.
Zhaolei ZhangThe Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Ontario, Canada.
Lorne ZinmanSunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada.
Jonathan Daniel RohrerDementia Research Centre, University College London, London, UK.
Maria Carmela TartagliaTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.
Janice RobertsonDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Genetic FTD Initiative (GENFI)
University of Toronto · CAUniversity of California, San Francisco · USSunnybrook Health Science Centre · CAErasmus MC · NLKarolinska Institutet · SEUK Dementia Research Institute · GBUniversité Laval · CAUniversity Health Network · CAUniversity of Brescia · ITUniversity of Milan · IT

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
Training - The Frontotemporal Lobar Degeneration Clinical Research ConsortiumU54NS092089 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2014 to 2018
$6.4M
Genetic Discovery and Pathobiology of Frontotemporal Lobar Degeneration and Related TDP-43 ProteinopathiesR35NS097261 · NINDS · MAYO CLINIC JACKSONVILLE · PI RADEMAKERS, ROSA · 2017 to 2019
$2.9M
CIHRDepartment of HealthMedical Research Council MC_U105597119Medical Research Council MC_UU_00005/12Medical Research Council MR/J009482/1Medical Research Council MR/M008525/1Medical Research Council MR/M023664/1NIA NIH HHS P01 AG019724NIA NIH HHS P50 AG023501NIA NIH HHS R01 AG038791NINDS NIH HHS R35 NS097261NINDS NIH HHS U54 NS092089
6 · The paper itself

Abstract

objectiveTo determine whether exosomal microRNAs (miRNAs) in cerebrospinal fluid (CSF) of patients with frontotemporal dementia (FTD) can serve as diagnostic biomarkers, we assessed miRNA expression in the Genetic Frontotemporal Dementia Initiative (GENFI) cohort and in sporadic FTD.

methodsGENFI participants were either carriers of a pathogenic mutation in progranulin, chromosome 9 open reading frame 72 or microtubule-associated protein tau or were at risk of carrying a mutation because a first-degree relative was a known symptomatic mutation carrier. Exosomes were isolated from CSF of 23 presymptomatic and 15 symptomatic mutation carriers and 11 healthy non-mutation carriers. Expression of 752 miRNAs was measured using quantitative PCR (qPCR) arrays and validated by qPCR using individual primers. MiRNAs found differentially expressed in symptomatic compared with presymptomatic mutation carriers were further evaluated in a cohort of 17 patients with sporadic FTD, 13 patients with sporadic Alzheimer's disease (AD) and 10 healthy controls (HCs) of similar age.

resultsIn the GENFI cohort, miR-204-5p and miR-632 were significantly decreased in symptomatic compared with presymptomatic mutation carriers. Decrease of miR-204-5p and miR-632 revealed receiver operator characteristics with an area of 0.89 (90% CI 0.79 to 0.98) and 0.81 (90% CI 0.68 to 0.93), respectively, and when combined an area of 0.93 (90% CI 0.87 to 0.99). In sporadic FTD, only miR-632 was significantly decreased compared with AD and HCs. Decrease of miR-632 revealed an area of 0.90 (90% CI 0.81 to 0.98).

conclusionsExosomal miR-204-5p and miR-632 have potential as diagnostic biomarkers for genetic FTD and miR-632 also for sporadic FTD.

Indexed as

Down-RegulationBiomarkersExosomesFemaleFrontotemporal DementiaHumansMaleMicroRNAstau ProteinsBiomarkersMicroRNAsMIRN204 microRNA, humanMIRN632 microRNA, humantau Proteins

Identifiers

PMID29434051
PMCPMC6045452
OpenAlexW2786653123

What OpenQuestion holds

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LicenceCC BY
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.