Evidence map›Paper›PMID 30697364›Full record

ArticleInternational journal of physiology, pathophysiology and pharmacology2018

Profiling of Argonaute-2-loaded microRNAs in a mouse model of frontotemporal dementia with parkinsonism-17.

Aidan Kenny, Félix Hernández, Jesús Avila, José J Lucas, David C Henshall, Jochen Hm Prehn, Eva M Jiménez-Mateos, Tobias Engel

Open access · greenAbstract read
In one paragraph

Article in International journal of physiology, pathophysiology and pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

8 authors at 3 institutions in 2 countries.

Aidan KennyDepartment of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.
Félix HernándezDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa", Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED) Madrid, Spain.
Jesús AvilaDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa", Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED) Madrid, Spain.
José J LucasDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa", Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED) Madrid, Spain.
David C HenshallDepartment of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.
Jochen Hm PrehnDepartment of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.
Eva M Jiménez-MateosDepartment of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.
Tobias EngelDepartment of Physiology and Medical Physics, Royal College of Surgeons in Ireland Dublin 2, Ireland.
Royal College of Surgeons in Ireland · IEUnidades Centrales Científico-Técnicas · ESConsejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tauopathies are a group of neurodegenerative diseases characterized by the pathological aggregation of the microtubule-associated protein tau. These include more than 20 diseases, with Alzheimer's disease being the most frequent. While pathological and neurotoxic effects of tau are well documented, the mechanisms by which tau can promote neurodegeneration are less clear. Increasing evidence suggests a functional role for microRNAs in the pathogenesis of tauopathies, with altered expression and function of microRNAs in experimental models and patient brain. To determine whether a pathological expression of tau leads to altered microRNA expression, we investigated a mouse model (VLW), which overexpresses tau carrying three mutations identified in patients suffering from frontotemporal dementia with parkinsonism-17. Argonaute-2-bound microRNAs were co-immunoprecipitated using hippocampal tissue to identify active microRNAs within the model and quantified using a genome-wide high-throughput qPCR-based microRNA platform. While similar numbers of microRNAs are present between wild-type and VLW mice, a prominent increase in Argonaute-2-bound levels of microRNAs could be observed in VLW mice. This included microRNA-134, microRNA-99a and microRNA-101. Subsequent experiments revealed this increase in Argonaute-2 loading of microRNAs to correlate with increased microRNA expression. Our

Indexed as

Argonaute-2frontotemporal dementia with parkinsonism-17MicroRNATauopathy

Identifiers

PMID30697364
PMCPMC6334219
OpenAlexW3022877761

What OpenQuestion holds

Textmetadata
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.