Evidence map›Paper›PMID 32950103›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021

miR-204-3p/Nox4 Mediates Memory Deficits in a Mouse Model of Alzheimer's Disease.

Wenyuan Tao, Linjie Yu, Shu Shu, Ying Liu, Zi Zhuang, Siyi Xu, Xinyu Bao, Yue Gu, Fang Cai, Weihong Song and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Wenyuan TaoDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Linjie YuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Shu ShuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Ying LiuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Zi ZhuangDepartment of Neurology, Drum Tower Hospital of Nanjing Medical University, Nanjing, Jiangsu 211166, PR China.
Siyi XuDepartment of Neurology, Drum Tower Hospital of Nanjing Medical University, Nanjing, Jiangsu 211166, PR China.
Xinyu BaoDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Yue GuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China.
Fang CaiTownsend Family Laboratories, Department of Psychiatry, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Weihong SongTownsend Family Laboratories, Department of Psychiatry, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Yun XuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China; Department of Neurology, Drum Tower Hospital of Nanjing Medical University, Nanjing, Jiangsu 211166, PR China. Electronic address: xuyun20042001@aliyun.com.
Xiaolei ZhuDepartment of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu 210008, PR China; Institute of Brain Sciences, Nanjing University, Nanjing, Jiangsu 210093, PR China; Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing, Jiangsu 210008, PR China; Jiangsu Province Stroke Center for Diagnosis and Therapy, Nanjing, Jiangsu 210008, PR China; Nanjing Neuropsychiatry Clinic Medical Center, Nanjing, Jiangsu 210008, PR China; Department of Neurology, Drum Tower Hospital of Nanjing Medical University, Nanjing, Jiangsu 211166, PR China. Electronic address: zhuquelee@126.com.
Jiangsu Province Blood Center · CNNanjing University · CNNanjing Drum Tower Hospital · CNUniversity of British Columbia · CANanjing Medical University · CN

Funding

CIHR PJT-166127
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder leading to dementia in the elderly, and the mechanisms of AD are not fully defined. MicroRNAs (miRNAs) have been shown to contribute to memory deficits in AD. In this study, we identified that miR-204-3p was downregulated in the hippocampus and plasma of 6-month-old APPswe/PS1dE9 (APP/PS1) mice. miR-204-3p overexpression attenuated memory and synaptic deficits in APP/PS1 mice. The amyloid levels and oxidative stress were decreased in the hippocampus of APP/PS1 mice after miR-204-3p overexpression. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (Nox4) was a target of miR-204-3p, and Nox4 inhibition by GLX351322 protected neuronal cells against Aβ

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersDisease Models, AnimalDisease SusceptibilityMemory DisordersMiceMice, TransgenicMicroRNAsNADPH Oxidase 4Oxidative StressAmyloid beta-PeptidesBiomarkersMicroRNAsMIRN204 microRNA, mouseNADPH Oxidase 4Nox4 protein, mouseAlzheimer’s diseasebeta amyloidmemory deficitsmiR-204-3pNox4oxidative stresssynaptic dysfunction

Identifiers

PMID32950103
PMCPMC7791017
OpenAlexW3083148784

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.