Evidence map›Paper›PMID 27458373›Full record

ArticleFrontiers in aging neuroscience2016

Role of miR-211 in Neuronal Differentiation and Viability: Implications to Pathogenesis of Alzheimer's Disease.

Chunying Fan, Qi Wu, Xiaoyang Ye, Hongxue Luo, Dongdong Yan, Yi Xiong, Haili Zhu, Yarui Diao, Wei Zhang, Jun Wan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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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 2 institutions in 4 countries.

Chunying FanShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Qi WuShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Xiaoyang YeShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Hongxue LuoShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Dongdong YanShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Yi XiongShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Haili ZhuShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Yarui DiaoLudwig Institute for Cancer Research, La Jolla CA, USA.
Wei ZhangShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical Center Shenzhen, China.
Jun WanShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen-Peking University-The Hong Kong University of Science and Technology Medical CenterShenzhen, China; Division of Life Science, The Hong Kong University of Science and TechnologyHong Kong, China.
Hong Kong University of Science and Technology · HKLudwig Cancer Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related irreversible neurodegenerative disorder characterized by extracellular β Amyloid(Aβ) deposition, intracellular neurofibrillary tangles and neuronal loss. The dysfunction of neurogenesis and increased degeneration of neurons contribute to the pathogenesis of AD. We now report that miR-211-5p, a small non-coding RNA, can impair neurite differentiation by directly targeting NUAK1, decrease neuronal viability and accelerate the progression of Aβ-induced pathologies. In this study, we observed that during embryonic development, the expression levels of miR-211-5p were down-regulated in the normal cerebral cortexes of mice. However, in APPswe/PS1ΔE9 double transgenic adult mice, it was up-regulated from 9 months of age compared to that of the age-matched wild type mice. Studies in primary cortical neuron cultures demonstrated that miR-211-5p can inhibit neurite growth and branching via NUAK1 repression and decrease mature neuron viability. The impairments were more obvious under the action of Aβ. Our data showed that miR-211-5p could inhibit cortical neuron differentiation and survival, which may contribute to the synaptic failure, neuronal loss and cognitive dysfunction in AD.

Indexed as

Alzheimer’s disease (AD)amyloid β (Aβ)microRNA-211-5pneurite branchingneuronal viabilityNUAK1

Identifiers

PMID27458373
PMCPMC4937029
OpenAlexW2469757907

What OpenQuestion holds

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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.