ArticleYonsei medical journal2018
Inhibition of miR-128 Abates Aβ-Mediated Cytotoxicity by Targeting PPAR-γ via NF-κB Inactivation in Primary Mouse Cortical Neurons and Neuro2a Cells.
Article in Yonsei medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Prediction of differentially expressed microRNAs in blood as potential biomarkers for Alzheimer's disease by meta-analysis and adaptive boosting ensemble learning.Alzheimer's research & therapy · 2021Pooled it
- Interplay between brain-specific microRNAs and Alzheimer's disease.Neural regeneration research · 2026Article
- Electrochemical detection of miRNA-128 in Alzheimer's disease using (3-aminopropyl) triethoxysilane and citrate-capped green-synthesized silver nanoparticles.Mikrochimica acta · 2026Article
- Literature-derived serum miRNA signatures associated with cognitive decline in Alzheimer's disease: integrated analysis and machine learning-based diagnostic modeling.Alzheimer's research & therapy · 2026Article
- Uncovering the role of integrated stress in Alzheimer's disease through single-cell and transcriptomic analysis.Scientific reports · 2026Article
- MicroRNA Signatures in Alzheimer's Disease and Normal-Tension Glaucoma: A Comparative Expression Analysis of miR-128 and miR-455-3p.Current Alzheimer research · 2026Article
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- Therapeutic potential and microRNA regulating properties of phytochemicals in Alzheimer's disease.Molecular therapy. Nucleic acids · 2025Review
- Article
- Fetal Brain-Derived Exosomal miRNAs from Maternal Blood: Potential Diagnostic Biomarkers for Fetal Alcohol Spectrum Disorders (FASDs).International journal of molecular sciences · 2024Article
- MiR-128-3p - a gray eminence of the human central nervous system.Molecular therapy. Nucleic acids · 2024Review
- Understanding the multifaceted role of miRNAs in Alzheimer's disease pathology.Metabolic brain disease · 2024Review
- Bergenin mitigates neuroinflammatory damage induced by high glucose: insights from Zebrafish, murine microbial cell line, and rat models.Frontiers in pharmacology · 2024Article
- Discerning the Prospects of miRNAs as a Multi-Target Therapeutic and Diagnostic for Alzheimer's Disease.Molecular neurobiology · 2023Review
- Non-Coding RNA in Microglia Activation and Neuroinflammation in Alzheimer's Disease.Journal of inflammation research · 2023Review
- 3D genome-selected microRNAs to improve Alzheimer's disease prediction.Frontiers in neurology · 2023Article
- MicroRNAs in Learning and Memory and Their Impact on Alzheimer's Disease.Biomedicines · 2022Review
- Dysregulated miRNAs as Biomarkers and Therapeutical Targets in Neurodegenerative Diseases.Journal of personalized medicine · 2022Review
- Role of miRNAs in Neurodegeneration: From Disease Cause to Tools of Biomarker Discovery and Therapeutics.Genes · 2022Review
- Brain-enriched miR-128: Reduced in exosomes from Parkinson's patient plasma, improves synaptic integrity, and prevents 6-OHDA mediated neuronal apoptosis.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlzheimer's disease (AD) is the sixth most common cause of death in the United States. MicroRNAs have been identified as vital players in neurodegenerative diseases, including AD. microRNA-128 (miR-128) has been shown to be dysregulated in AD. This study aimed to explore the roles and molecular mechanisms of miR-128 in AD progression. MATERIALS AND
methodsExpression patterns of miR-128 and peroxisome proliferator-activated receptor gamma (PPAR-γ) messenger RNA in clinical samples and cells were measured using RT-qPCR assay. PPAR-γ protein levels were determined by Western blot assay. Cell viability was determined by MTT assay. Cell apoptotic rate was detected by flow cytometry via double-staining of Annexin V-FITC/PI. Caspase 3 and NF-κB activity was determined by a Caspase 3 Activity Assay Kit or NF-κB p65 Transcription Factor Assay Kit, respectively. Bioinformatics prediction and luciferase reporter assay were used to investigate interactions between miR-128 and PPAR-γ 3'UTR.
resultsMiR-128 expression was upregulated and PPAR-γ expression was downregulated in plasma from AD patients and amyloid-β (Aβ)-treated primary mouse cortical neurons (MCN) and Neuro2a (N2a) cells. Inhibition of miR-128 decreased Aβ-mediated cytotoxicity through inactivation of NF-κB in MCN and N2a cells. Moreover, PPAR-γ was a target of miR-128. PPAR-γ upregulation attenuated Aβ-mediated cytotoxicity by inactivating NF-κB in MCN and N2a cells. Furthermore, PPAR-γ downregulation was able to abolish the effect of anti-miR-128 on cytotoxicity and NF-κB activity in MCN and N2a cells.
conclusionMiR-128 inhibitor decreased Aβ-mediated cytotoxicity by upregulating PPAR-γ via inactivation of NF-κB in MCN and N2a cells, providing a new potential target in AD treatment.
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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.