ArticleGalen medical journal2023
Potential Regulatory Role of miR-21 on Alzheimer's Disease by Targeting GSK-3β Signaling.
Article in Galen medical journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- miR-584-5p suppresses AβActa neurologica Belgica · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is the most important neurogenerative disorder with progressive dementia as its main clinical manifestation. The microRNAs (miRNAs) are identified as crucial modulators in AD progression. Nevertheless, the biological potential of miR-21 in AD is obscure. Hence, this study aimed to evaluate the possible role of miR-21 in the pathogenesis of AD via phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3beta (GSK-3β) signaling. MATERIALS AND
methodsThe miR-21 expression in the brain tissues of patients with AD, as well as normal brain tissues and Aβ1-42-stimulated SH-SY5Y cell line (AD model) was examined by in situ hybridization and quantitative real-time polymerase chain reaction. Also, the apoptosis-linked protein levels as well as programmed cell death 4 (PDCD4) were detected by western blot.
resultsOur findings revealed that miR-21 was low expressed in the brain tissues of patients with AD and AD model (P0.01). Also, the miR-21 overexpression could inhibit apoptosis of the AD model (P0.01). Indeed, the miR-21 negatively regulated PDCD4 expression, which led to activated PI3K/AKT/GSK-3β signaling.
conclusionOur study demonstrated that miR-21 cloud inhibits cell apoptosis in AD through the activation of PI3K/AKT/GSK-3β signaling pathway using inhibition of PDCD4 expression.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.