Evidence map›Paper›PMID 22043907›Full record

ArticleJournal of toxicology and environmental health. Part A2011

Upregulation of micro RNA-146a (miRNA-146a), a marker for inflammatory neurodegeneration, in sporadic Creutzfeldt-Jakob disease (sCJD) and Gerstmann-Straussler-Scheinker (GSS) syndrome.

W J Lukiw, P Dua, A I Pogue, C Eicken, J M Hill

Abstract read
In one paragraph

Article in Journal of toxicology and environmental health. Part A, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

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  14. microRNA-146a-5p, Neurotropic Viral Infection and Prion Disease (PrD).International journal of molecular sciences · 2021
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7 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

W J LukiwLSU Neuroscience Center and Departments of Ophthalmology, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, LA70112-2272, USA. wlukiw@lsuhsc.edu
P Dua
A I Pogue
C Eicken
J M Hill
Louisiana State University Health Sciences Center New Orleans · USLouisiana Tech University · USNorgen Biotek Corporation (Canada) · CA

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
microRNA (miRNA) signaling in Alzheimer's disease(AD)R01AG038834 · NIA · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2011 to 2020
$3.3M
Gene Expression in Alzheimer's DiseaseR01AG018031 · NIA · LSU HEALTH SCIENCES CENTER · PI LUKIW, WALTER J · 2001 to 2006
$1.4M
NIA NIH HHS NIA AG038834NIA NIH HHS NIA AG18031NIA NIH HHS P50 AG016573NIA NIH HHS P50 AG16573NIA NIH HHS R01 AG018031NIA NIH HHS R01 AG038834
6 · The paper itself

Abstract

A mouse- and human-brain-abundant, nuclear factor (NF)-кB-regulated, micro RNA-146a (miRNA-146a) is an important modulator of the innate immune response and inflammatory signaling in specific immunological and brain cell types. Levels of miRNA-146a are induced in human brain cells challenged with at least five different species of single- or double-stranded DNA or RNA neurotrophic viruses, suggesting a broad role for miRNA-146a in the brain's innate immune response and antiviral immunity. Upregulated miRNA-146a is also observed in pro-inflammatory cytokine-, Aβ42 peptide- and neurotoxic metal-induced, oxidatively stressed human neuronal-glial primary cell cocultures, in murine scrapie and in Alzheimer's disease (AD) brain. In AD, miRNA-146a levels are found to progressively increase with disease severity and co-localize to brain regions enriched in inflammatory neuropathology. This study provides evidence of upregulation of miRNA-146a in extremely rare (incidence 1-10 per 100 million) human prion-based neurodegenerative disorders, including sporadic Creutzfeldt-Jakob disease (sCJD) and Gerstmann-Straussler-Scheinker syndrome (GSS). The findings suggest that an upregulated miRNA-146a may be integral to innate immune or inflammatory brain cell responses in prion-mediated infections and to progressive and irreversible neurodegeneration of both the murine and human brain.

Indexed as

Amyloid beta-PeptidesAnimalsBrainCells, CulturedCreutzfeldt-Jakob SyndromeGerstmann-Straussler-Scheinker DiseaseHumansMiceMicroRNAsNeurogenic InflammationNeuronsPeptide FragmentsUp-RegulationAmyloid beta-Peptidesamyloid beta-protein (1-42)MicroRNAsMIRN146 microRNA, humanPeptide Fragments

Identifiers

PMID22043907
PMCPMC3719866
OpenAlexW2057231053

What OpenQuestion holds

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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.