Evidence map›Paper›PMID 34540002›Full record

ArticleAmerican journal of translational research2021

LncRNA NEAT1 promotes Alzheimer's disease by down regulating micro-27a-3p.

Li-Xia Dong, Yan-Yun Zhang, Hai-Lan Bao, Yu Liu, Guo-Wei Zhang, Feng-Mao An

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  9. LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025
    Review
  10. Article
  11. Article
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  14. Article
  15. Tanshinone IIA improves Alzheimer's diseaseWorld journal of psychiatry · 2024
    Article
  16. [Expression relationship and significance of NEAT1 and miR-27a-3p in serum and cerebrospinal fluid of patients with Alzheimer disease].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
    Article
  17. 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

6 authors at 1 institution in 1 country.

Li-Xia DongCollege of Nursing, Inner Mongolia University for Nationalities Tongliao 028000, Inner Mongolia Autonomous Region, P. R. China.
Yan-Yun ZhangCollege of Nursing, Inner Mongolia University for Nationalities Tongliao 028000, Inner Mongolia Autonomous Region, P. R. China.
Hai-Lan BaoCollege of Nursing, Inner Mongolia University for Nationalities Tongliao 028000, Inner Mongolia Autonomous Region, P. R. China.
Yu LiuCollege of Nursing, Inner Mongolia University for Nationalities Tongliao 028000, Inner Mongolia Autonomous Region, P. R. China.
Guo-Wei ZhangCollege of Nursing, Inner Mongolia University for Nationalities Tongliao 028000, Inner Mongolia Autonomous Region, P. R. China.
Feng-Mao AnInstitute of Dementia, Inner Mongolia University for Nationalities Tongliao, Inner Mongolia, P. R. China.
Inner Mongolia University for Nationalities · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAlzheimer's disease (AD) is a common neurodegenerative disease. This study was designed to investigate the roles of lncRNA NEAT1/miR-27a-3p axis in AD.

methodsAmyloid protein was used to treat SH-SY5Y cells and rats to construct AD model. RT-qPCR was used to quantify lncRNA NEAT1 and micro-27a-3p in AD model cells. Western blot was used to determine the β-amyloid-precursor-protein-cleaver-enzyme 1 (BACE1), amyloid, Tau protein and its phosphorylation, Caspase 3 protein and its lytic cell protein and amyloid precursor protein (APP). Flow cytometry was used to detect apoptosis. The cell activity was detected by CCK-8. The lncRNA NEAT1 and miR-27a-3p inhibition or over-expression vectors were constructed. The dual luciferase reporter gene and RNA pull-down assay were used to detect the targeting relationship between lncRNA NEAT1 and micro-27a-3p. The cognitive function of rats was tested by water maze.

resultsAfter being induced by amyloid protein, lncRNA NEAT1 was up-regulated while micro-27a-3p was down-regulated in SH-SY5Y cells. Apoptosis rate was increased and cell activity was decreased. Amyloid protein, BACE1 protein, APP protein, Tau protein and its phosphorylation, Caspase 3 protein and its lytic cell protein were up-regulated. Down-regulation of lncRNA NEAT1 or up-regulation of micro-27a-3p could reduce cell apoptosis, increase cell activity, down-regulate amyloid protein, BACE1 protein, APP protein, Tau protein and its phosphorylation, and up-regulate caspase 3 protein and its lysate protein. Dual luciferase reporter gene assay and RNA pull-down experiments revealed that micro-27a-3p was the target gene of lncRNA NEAT1. Down-regulation of micro-27a-3p could offset the changes caused by LncRNA NEAT1. AD caused cognitive dysfunction in rats, which was improved by down-regulation of lncRNA NEAT1.

conclusionlncRNA NEAT1 regulates the development of AD by down-regulating micro-27a-3p.

Indexed as

Alzheimer’s diseaselncRNA NEAT1miR-27a-3p

Identifiers

PMID34540002
PMCPMC8430163
OpenAlexW3199044223

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.