Evidence map›Paper›PMID 37192007›Full record

ArticleJCI insight2023

MiR-431 attenuates synaptic plasticity and memory deficits in APPswe/PS1dE9 mice.

Jianwei Ge, Zhiwei Xue, Shu Shu, Linjie Yu, Ruomeng Qin, Wenyuan Tao, Pinyi Liu, Xiaohong Dong, Zhen Lan, Xinyu Bao and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  12. Progressive reduction of nuclear receptor Nr4a1 mediates age-dependent cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  13. A state-of-the-art review on miRNA in prevention and treatment of AlzheimerZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Review
  14. 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

13 authors at 3 institutions in 2 countries.

Jianwei GeDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Zhiwei XueDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Shu ShuDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Linjie YuDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Ruomeng QinDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Wenyuan TaoDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Pinyi LiuDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Xiaohong DongDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Zhen LanDepartment of Neurology, Drum Tower Hospital of Nanjing Medical University, Nanjing, China.
Xinyu BaoDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Lei YeDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Yun XuDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Xiaolei ZhuDepartment of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School.
Nanjing Drum Tower Hospital · CNNanjing University · CNPharmaceutical Biotechnology (Czechia) · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), and emerging evidence has shown that microRNAs (miRs) are alternative biomarkers and therapeutic targets for synaptic dysfunctions in AD. In this study, we found that the level of miR-431 was downregulated in the plasma of patients with amnestic mild cognitive impairment and AD. In addition, it was decreased in the hippocampus and plasma of APPswe/PS1dE9 (APP/PS1) mice. Lentivirus-mediated miR-431 overexpression in the hippocampus CA1 ameliorated synaptic plasticity and memory deficits of APP/PS1 mice, while it did not affect amyloid-β levels. Smad4 was identified as a target of miR-431, and Smad4 knockdown modulated the expression of synaptic proteins, including SAP102, and protected against synaptic plasticity and memory dysfunctions in APP/PS1 mice. Furthermore, Smad4 overexpression reversed the protective effects of miR-431, indicating that miR-431 attenuated synaptic impairment at least partially by Smad4 inhibition. Thus, these results indicated that miR-431/Smad4 might be a potential therapeutic target for AD treatment.

Indexed as

Alzheimer DiseaseMicroRNAsAnimalsMemory DisordersMiceMice, TransgenicNeuronal PlasticityMicroRNAsMIRN431 microRNA, mouseAgingNeurodegenerationTherapeutics

Identifiers

PMID37192007
PMCPMC10371242
OpenAlexW4376643018

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.