Evidence map›Paper›PMID 25148207›Full record

ArticlePloS one2014

Genome-wide analysis of miRNA signature in the APPswe/PS1ΔE9 mouse model of alzheimer's disease.

Hongxue Luo, Qi Wu, Xiaoyang Ye, Yi Xiong, Jinyong Zhu, Junyu Xu, Yarui Diao, Duo Zhang, Maosheng Wang, Jinhua Qiu and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Frontiers in molecular neuroscience · 2017
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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

13 authors at 5 institutions in 3 countries.

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, Guangdong Province, 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, Guangdong Province, 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, Guangdong Province, 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, Guangdong Province, China.
Jinyong ZhuShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China.
Junyu XuShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China.
Yarui DiaoLudwig Institute for Cancer Research, La Jolla, California, United States of America.
Duo ZhangDepartment of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, California, United States of America.
Maosheng WangGaoZhou people's Hospital, Gao Zhou, Guangdong Province, China.
Jinhua QiuGaoZhou people's Hospital, Gao Zhou, Guangdong Province, China.
Jianting MiaoDepartment of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi'an City, Shanxi Province, China.
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, Guangdong Province, China.
Jun WanShenzhen Key Laboratory for Neuronal Structural Biology, Biomedical Research Institute, Shenzhen Peking University - The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China; Division of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Hong Kong University of Science and Technology · HKGaozhou People's Hospital · CNAir Force Medical University · CNLudwig Cancer Research · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia. One of the pathological hallmarks of AD is amyloid β (Aβ) deposition. MicroRNAs (miRNAs) are small non-coding RNAs whose expression levels change significantly during neuronal pathogenesis and may be used as diagnostic markers. Some miRNAs are important in AD development by targeting genes responsible for Aβ metabolism. However, a systematic assessment of the miRNA expression profile induced by Aβ-mediated neuronal pathogenesis is still lacking. In the present study, we examined miRNA expression profile by using the APPswe/PS1ΔE9 mouse model of AD. Two sibling pairs of mice were examined, showing 30 and 24 miRNAs with significantly altered expression levels from each paired control, respectively. Nine known miRNAs were common in both groups. Prediction of putative target genes and functional annotation implied that these altered miRNAs affect many target genes mainly involved in PI3K/Akt signaling pathway. This study provides a general profile of miRNAs regulated by Aβ-associated signal pathways, which is helpful to understand the mechanism of Aβ-induced neuronal dysfunction in AD development.

Indexed as

Genome-Wide Association StudyTranscriptomeAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrainComputational BiologyDisease Models, AnimalGene Expression ProfilingGene Expression RegulationMiceMice, TransgenicMicroRNAsMolecular Sequence AnnotationPhosphatidylinositol 3-KinasesPresenilin-1Amyloid beta-Protein PrecursorMicroRNAsPhosphatidylinositol 3-KinasesPresenilin-1Proto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID25148207
PMCPMC4141691
OpenAlexW2072925645

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.