Evidence map›Paper›PMID 31134481›Full record

ArticleMetabolic brain disease2019

Intrahippocampal miR-342-3p inhibition reduces β-amyloid plaques and ameliorates learning and memory in Alzheimer's disease.

Yin Fu, Xiaoyang Hu, Chunyu Zheng, Guicai Sun, Jianyu Xu, Shanshan Luo, Peigang Cao

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  4. MicroRNA cargo in neuron-derived vesicles as peripheral biomarkers of brain insulin dysregulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

7 authors at 4 institutions in 1 country.

Yin FuHeilongjiang University of Chinese Medicine, Harbin, 150040, China.
Xiaoyang HuBasic Medical College of Heilongjiang University of Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Chunyu ZhengHeilongjiang University of Chinese Medicine, Harbin, 150040, China.
Guicai SunDepartment of Orthopaedics, The Fourth Affiliated Hospital of Nanchang University, Jiangxi, 330003, China.
Jianyu XuDepartment of Radiation Oncology, Tumor Hospital of Harbin Medical University, Harbin, 150000, China.
Shanshan LuoDepartment of Pharmacy, No.211 Hospital of PLA, Harbin, 50000, China.
Peigang CaoDepartment of Cardiology, General Hospital of Heilongjiang Agricultural Reclamation Bureau, No. 235 Hashuang Road, Harbin, 150088, Heilongjiang Province, China. caopeigang@126.com.
Heilongjiang University of Chinese Medicine · CNHeilongjiang Academy of Land Reclamation Sciences · CNNanchang University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of extracellular amyloid-β (Aβ) in hippocampal subregions is a hallmark of Alzheimer's disease (AD), which promotes neuronal apoptosis, potentiates cognitive decline and play a causative role in AD pathogenesis. However, whether this process is controlled by distinct miRNAs at the posttranscriptional level remain fascinating but poorly understood. Using post mortem hippocampal samples from human AD patients and 3xTg-AD mouse, we demonstrate that miR-342-3p expression was significantly induced during the AD development. With the aid of intrahippocampal injection of miR-342-3p antagomir, we further show that in vivo miR-342-3p inhibition synergistically improved cognitive deficits in 3xTg-AD mice. The hippocampal Aβ-plaque burden in 3xTg-AD mice, as revealed by immunohistochemical analysis with 4G8 antibody, was attenuated also. Mechanistically, the upregulation of neuronal miR-342-3p is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons in Aβ-challenged HT22 hippocampal neuronal cells. These findings support the model that derangement of hippocampus signal transduction and subsequent neuronal apoptosis in AD arises as a consequence of increased Aβ burden and chronic activation of the JNK MAPK cascade in a miR-342-3p-dependent manner. Overall, we described for the first time the regulatory activity of miR-342-3p on relevant Aβ metabolism pathways in Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsAntagomirsCell LineFemaleHippocampusHumansLearningMaleMemoryMiceMice, TransgenicMicroRNAsNeuronsPlaque, AmyloidSignal TransductionAntagomirsMicroRNAsMirn342 microRNA, mouseAlzheimer’s disease (AD)Amyloid-βApoptosisJNKMicroribonucleic acids (miRNAs)

Identifiers

PMID31134481
OpenAlexW2947026164

What OpenQuestion holds

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Read underepoch 390

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.