ArticleAnnals of translational medicine2022
A study on the neuroprotective effect of miR-206-3p on Alzheimer's disease mice by regulating brain-derived neurotrophic factor.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- MicroRNAs modulation by curcumin, catalpol, and other natural products in Alzheimer's disease: a review.Molecular biology reports · 2025Review
- Evidence for the Contribution of the miR-206/BDNF Pathway in the Pathophysiology of Depression.The international journal of neuropsychopharmacology · 2024Review
- Insights into the Role of microRNAs as Clinical Tools for Diagnosis, Prognosis, and as Therapeutic Targets in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- A Comprehensive Review on the Importance of MiRNA-206 in the Animal Model and Human Diseases.Current neuropharmacology · 2024Review
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- Promising Therapeutic Potential of miR-220-3p Mimic Against Murine Trimethyltin Hippocampal Injury.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Brain-derived neurotrophic factor (BDNF) is involved in the regulation of Alzheimer's disease (AD), but the mechanism is not clear. This study explores the possible mechanism of microRNA-206-3p (miR-206-3p) participating in the neuroprotective effect of AD mice by regulating BDNF. Methods: 36 SPF grade C57 mice were randomly divided into normal group, model group and miR-206-3p mimics group (intraperitoneal injection of 3 mm miR-206-3p mimics) (n=12). miR-206-3p mimics group was intervened by miR-206-3p mimics on the basis of AD model. The expression of miR-206-3p was detected by Real time quantitative polymerase chain reaction (qPCR). Zea-Longa score and water maze were used for behavioral detection, he was used to observe the morphology of neurons, and immunohistochemical Western blot was used to detect the expression of BDNF protein, and the targeting relationship between miR-206-3p and BDNF was analyzed. Results: Compared with the model group, the expression level of miR-206-3p in miR-206-3p mimics group was significantly higher (P<0.05). compared with the model group, the Zea-Longa score in miR-206-3p mimics group was significantly lower (P<0.05). The escape latency of miR-206-3p mimics group was significantly shorter than that of model group, and the number of crossing the original platform was significantly more than that of model group (P<0.05). The morphology of neurons in miR-206-3p mimics group was significantly better than that in model group; Immunohistochemistry and Western blot showed that the relative expression of miR-206-3p mimics BDNF protein was significantly increased compared with the model group (P<0.05). Compared with miR-206-3p control group, the luciferase activity at 3' end untranslated area (3' UTR) end of wild-type BDNF in miR-206-3p inhibition group decreased significantly (P<0.01). Conclusions: miR-206-3p exerts neuroprotective effects on AD mouse neurons by up-regulating BDNF.
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