ArticleMolecular genetics & genomic medicine2021
MiR-485-3p serves as a biomarker and therapeutic target of Alzheimer's disease via regulating neuronal cell viability and neuroinflammation by targeting AKT3.
Article in Molecular genetics & genomic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Malvidin and Its Mono- and Di-Glucosides Forms: A Study of Combining Both In Vitro and Molecular Docking Studies Focused on Cholinesterase, Butyrylcholinesterase, COX-1 and COX-2 Activities.Molecules (Basel, Switzerland) · 2023Article
- Role of non‑coding RNAs as biomarkers and the application of omics technologies in Alzheimer's disease (Review).International journal of molecular medicine · 2023Review
- miR-212-3p attenuates neuroinflammation of rats with Alzheimer's disease via regulating the SP1/BACE1/NLRP3/Caspase-1 signaling pathway.Bosnian journal of basic medical sciences · 2022Article
- Diagnostic Performance of miR-485-3p in Patients with Parkinson's Disease and its Relationship with Neuroinflammation.Neuromolecular medicine · 2022Article
- MicroRNA Alteration, Application as Biomarkers, and Therapeutic Approaches in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases.Frontiers in neurology · 2022Review
- Combinational treatments of RNA interference and extracellular vesicles in the spinocerebellar ataxia.Frontiers in molecular neuroscience · 2022Review
- Targeting MicroRNA-485-3p Blocks Alzheimer's Disease Progression.International journal of molecular sciences · 2021Article
- miRNAs as Therapeutic Tools in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Circulating miRNAs as Potential Biomarkers Distinguishing Relapsing-Remitting from Secondary Progressive Multiple Sclerosis. A Review.International journal of molecular sciences · 2021Review
- Key Disease Mechanisms Linked to Alzheimer's Disease in the Entorhinal Cortex.International journal of molecular sciences · 2021Article
- News about the Role of Fluid and Imaging Biomarkers in Neurodegenerative Diseases.Biomedicines · 2021Review
- Review
- Trabecular Bone Microarchitecture Improvement Is Associated With Skeletal Nerve Increase Following Aerobic Exercise Training in Middle-Aged Mice.Frontiers in physiology · 2021Article
- The Eminent Role of microRNAs in the Pathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
Corrections and comments
- Retraction · 2021-12-06Results Not Reproducible · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNumerous microRNAs (miRNAs) have been identified as functional molecules in Alzheimer's disease (AD) pathogenesis. This study aimed to investigate the diagnostic value of microRNA-485-3p (miR-485-3p) in AD patients, evaluate the effect of miR-485-3p on neuronal viability and neuroinflammation, as well as the underlying molecular mechanisms.
methodsQuantitative Real-Time PCR was used to estimate expression of miR-485-3p and AKT3. A ROC analysis was used to evaluate the diagnostic value of miR-485-3p. The correlation of miR-485-3p with patients' MMSE score and inflammatory response was analyzed. Using Aβ-treated SH-SY5Y and BV2 cells models, the effects of miR-485-3p on neuronal proliferation, apoptosis, and neuroinflammation were explored. A luciferase reporter assay was used to confirm the target gene of miR-485-3p in both SH-SY5Y and BV2 cells.
resultsSerum miR-485-3p expression was significantly upregulated in AD patients and cell models, which had a high diagnostic accuracy and correlated with MMSE score and inflammatory response in AD patients. The knockdown of miR-485-3p in SH-SY5Y and BV2 cells was found to significantly reverse the effect of Aβ treatment on neuronal viability and neuroinflammation. AKT3 was determined as a target of miR-485-3p, which might mediate the biological function of miR-485-3p in AD pathogenesis.
conclusionAll the data indicated that increased serum miR-485-3p serves as a diagnostic biomarker in AD patients, and knockdown of miR-485-3p exerts a neuroprotective role by improving neuronal viability and weakening neuroinflammation, which may be mediated by AKT3. This study may provide a novel biomarker and therapeutic target for AD therapy.
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