ArticleFrontiers in aging neuroscience2019
Loss of miR-369 Promotes Tau Phosphorylation by Targeting the Fyn and Serine/Threonine-Protein Kinase 2 Signaling Pathways in Alzheimer's Disease Mice.
Article in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 22 citations in OpenAlex.
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- Circular RNAs, miRNAs, and Exosomes: Their Roles and Importance in Amyloid-Beta and Tau Pathologies in Alzheimer's Disease.Neural plasticity · 2025Review
- The plasma miRNAome in ADNI: Signatures to aid the detection of at-risk individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Potential Application of MicroRNAs and Some Other Molecular Biomarkers in Alzheimer's Disease.Current issues in molecular biology · 2024Review
- Beyond CSF and Neuroimaging Assessment: Evaluating Plasma miR-145-5p as a Potential Biomarker for Mild Cognitive Impairment and Alzheimer's Disease.ACS chemical neuroscience · 2024Article
- Discerning the Prospects of miRNAs as a Multi-Target Therapeutic and Diagnostic for Alzheimer's Disease.Molecular neurobiology · 2023Review
- FYN: emerging biological roles and potential therapeutic targets in cancer.Journal of translational medicine · 2023Review
- A pathway analysis-based algorithm for calculating the participation degree of ncRNA in transcriptome.Scientific reports · 2022Article
- Treatment of Alzheimer's disease by combination of acupuncture and Chinese medicine based on pathophysiological mechanism: A review.Medicine · 2022Review
- MicroRNAs in the pathophysiology of Alzheimer's disease and Parkinson's disease: an overview.Molecular neurobiology · 2022Review
- Cerebrovascular microRNA Expression Profile During Early Development of Alzheimer's Disease in a Mouse Model.Journal of Alzheimer's disease : JAD · 2022Article
- Targeting the miRNA-155/TNFSF10 network restrains inflammatory response in the retina in a mouse model of Alzheimer's disease.Cell death & disease · 2021Article
- MicroRNAs as Potential Orchestrators of Alzheimer's Disease-Related Pathologies: Insights on Current Status and Future Possibilities.Frontiers in aging neuroscience · 2021Review
- SRPK2 Expression and Beta-Amyloid Accumulation Are Associated With BV2 Microglia Activation.Frontiers in integrative neuroscience · 2021Article
- Epigenetics: Recent Advances and Its Role in the Treatment of Alzheimer's Disease.Frontiers in neurology · 2020Review
- Advances and Challenges in Understanding MicroRNA Function in Tauopathies: A Case Study of miR-132/212.Frontiers in neurology · 2020Article
- Circulating Exosome microRNAs as Diagnostic Biomarkers of Dementia.Frontiers in aging neuroscience · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAlzheimer's disease (AD) is a progressive neurodegenerative dementia with the key pathological hallmarks amyloid-beta deposition and neurofibrillary tangles composed of hyperphosphorylated tau. microRNAs (miRNAs) are small non-coding RNAs that contribute to the pathogenesis of AD. In this study, we investigated the effect of the loss of miR-369 on the phosphorylation of tau protein and the activation of the kinases Fyn and serine/threonine-protein kinase 2 (SRPK2) as the upstream molecules facilitating tau phosphorylation in miR-369 knockout 3xTg-AD mice.
methodsWe generated miR-369 knockout 3xTg-AD mice and investigated their cognitive behaviors by maze tests. Real-time qPCR, western blot, and immunohistochemistry were performed to evaluate the expression of the miR-369 gene, phosphorylation of tau protein, and activation of Fyn and SRPK2. Luciferase reporter assays were applied to confirm the predicted targets of miR-369.
resultsKnocking out miR-369 in 3xTg AD mice aggravated cognitive impairment, promoted hyperphosphorylation of tau, and upregulated Fyn and SRPK2. Restoring miR-369 reversed the hyperphosphorylation of tau and downregulated Fyn and SRPK2. Additionally, miR-369 was shown to target the 3'UTRs of Fyn and SRPK2 to regulate their expression levels.
conclusionLoss of miR-369 promotes tau phosphorylation by targeting the Fyn and SRPK2 signaling pathways in AD mice, and supplementation with miR-369 might be a valuable option for AD therapeutic studies.
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