Evidence map›Paper›PMID 40820106›Full record

ArticleScientific reports2025

Regulatory role of LncRNA FMR1-AS1 in the pathogenesis of alzheimer's disease based on bioinformatics and in vitro experimental validation.

Xiang Yu, Hao Cai, Cai He, Zhong Ouyang, Yongchang Li, Liang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Article
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.

Xiang Yu *Department of Neurology, Hunan Provincial People's Hospital (First Affiliated Hospital of Hunan Normal University), No. 61 Jiefang West Road, Furong District, Changsha, 410005, Hunan Province, China.
Hao Cai *Department of Computer Science and Technology, College of Mathematics and Computer, Shantou University, Shantou, 515063, Guangdong, China.
Cai He *Department of Neurology, Hunan Provincial People's Hospital (First Affiliated Hospital of Hunan Normal University), No. 61 Jiefang West Road, Furong District, Changsha, 410005, Hunan Province, China.
Zhong Ouyang *Department of Computer Science and Technology, College of Mathematics and Computer, Shantou University, Shantou, 515063, Guangdong, China.
Yongchang LiDepartment of Neurology, Hunan Provincial People's Hospital (First Affiliated Hospital of Hunan Normal University), No. 61 Jiefang West Road, Furong District, Changsha, 410005, Hunan Province, China.
Liang ChenDepartment of Computer Science and Technology, College of Mathematics and Computer, Shantou University, Shantou, 515063, Guangdong, China. chenliang@stu.edu.cn.

Funding

Guangdong Province Special Fund for Science and Technology Project STKJ202209017Guangdong Science and Technology Plan Projects STKJ2023012National Natural Science Foundation of China 62002212National Science and Technology Major Project 2024ZD0529106Natural Science Foundation of Guang-dong Province 2025A1515012810
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a major cause of dementia, characterized by β-amyloid (Aβ) plaque accumulation and Tau protein hyperphosphorylation. Although long non-coding RNAs (lncRNAs) have been implicated in neurodegenerative diseases, their roles in AD remain unclear. This study analyzed RNA sequencing data from the brain tissues of 17 AD patients and 19 healthy controls (GEO: GSE138260) to construct a gene co-expression network and identified eight lncRNAs strongly associated with AD. FMR1-AS1 was selected for functional validation. In an Aβ1-42-induced SH-SY5Y neuronal injury model, overexpression of FMR1-AS1 significantly increased cell viability ([Formula: see text]), inhibited apoptosis ([Formula: see text]), and reduced Tau hyperphosphorylation ([Formula: see text]). FMR1-AS1 also alleviated oxidative stress by lowering reactive oxygen species (ROS) levels ([Formula: see text]), enhanced superoxide dismutase (SOD) activity ([Formula: see text]), and decreased malondialdehyde (MDA) content ([Formula: see text]). Knockdown of FMR1-AS1 exacerbated neuronal damage. These results demonstrate that FMR1-AS1 exerts neuroprotective effects by regulating apoptosis, oxidative stress, and Tau pathology. The study highlights FMR1-AS1 as a potential therapeutic target for AD and may advance the understanding of lncRNA-mediated regulatory mechanisms in neurodegeneration.

Indexed as

Alzheimer DiseaseFragile X Messenger Ribonucleoprotein 1RNA, Long NoncodingAgedAmyloid beta-PeptidesApoptosisCell Line, TumorCell SurvivalComputational BiologyFemaleGene Expression RegulationGene Regulatory NetworksHumansMaleNeuronsOxidative StressAmyloid beta-PeptidesFragile X Messenger Ribonucleoprotein 1Reactive Oxygen SpeciesRNA, Long Noncodingtau ProteinsAlzheimer’s diseaseAβ1–42BioinformaticsFMR1-AS1Neuronal cellsOxidative stressTau phosphorylation

Identifiers

PMID40820106
PMCPMC12358618

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