ArticleExperimental and therapeutic medicine2020
miR-132 improves the cognitive function of rats with Alzheimer's disease by inhibiting the MAPK1 signal pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Evidence of Clinical Efficacy and Pharmacological Mechanisms of Resveratrol in the Treatment of Alzheimer's Disease.Current Alzheimer research · 2023Pooled it
- UBA52 Overexpression Ameliorates Intracerebral Hemorrhage-Associated Neuronal Apoptosis and Mitochondrial Dysfunction: A Protective Role in Neurons.Molecular neurobiology · 2026Article
- Anti-senescence Effects of Nanovesicles Derived from Cluster of Differentiation-146-Positive Tonsil Mesenchymal Stem Cells via Modulation of the Tumor Protein 53 Pathway.Biomaterials research · 2026Article
- Effect of pyrogallol nanocomposite on miRNA and its associated pathways during radiation-induced toxicity in small intestine of irradiated Balb/C mice.Medical oncology (Northwood, London, England) · 2025Article
- Review
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- Neuroprotective Potential of Aminonaphthoquinone Derivatives Against Amyloid Beta-Induced Neuronal Cell Death Through Modulation of SIRT1 and BACE1.Neurochemical research · 2024Article
- miR-132-3p downregulatesThe Journal of international medical research · 2024Article
- 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
- MicroRNAs: pioneering regulators in Alzheimer's disease pathogenesis, diagnosis, and therapy.Translational psychiatry · 2024Review
- MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024Review
- NcRNAs: A synergistically antiapoptosis therapeutic tool in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- DNA hypomethylation promotes the expression of CASPASE-4 which exacerbates inflammation and amyloid-β deposition in Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Mesenchymal Stem Cells from Familial Alzheimer's Patients Express MicroRNA Differently.International journal of molecular sciences · 2024Article
- miR-129-5p as a biomarker for pathology and cognitive decline in Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Mechanism ofCurrent computer-aided drug design · 2024Article
- miR-129-5p as a biomarker for pathology and cognitive decline in Alzheimer's disease.Research square · 2023Article
- Identification ofInternational journal of molecular sciences · 2023Article
- A Study on Autophagy Related Biomarkers in Alzheimer's Disease Based on Bioinformatics.Cellular and molecular neurobiology · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a common worldwide progressive neurodegenerative disease. The dysregulation of miRNA is crucial in neurodegenerative diseases and neuron apoptosis during AD and is closely associated with the MAPK pathway. By bioinformatic website, we found that there was target inhibiting relationship between microRNA (miR)-132 and MAPK1. Therefore, the current study speculated that miR-132 could improve the cognitive function of rats with AD by inhibiting MAPK1 expression. To verify our hypothesis, 10 normal rats and 60 rats with AD were selected and divided into model, Ad-miR-132 negative control (NC), Ad-miR-132, Ad-small interfering (si)MAPK1 NC, Ad-siMAPK1 and Ad-miR-132 + Ad-MAPK1 groups. Rats were evaluated for learning by performing morris water maze tests and pathological changes of the hippocampus were assessed via HE staining. Additionally, hippocampus cell apoptosis was determined using a TUNEL assay and levels of acetylcholinesterase (AChE), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were evaluated in sera via ELISA. The mRNA and protein expression of miR-132, iNOS, MAPK1 and phosphorylated (p)-MAPK1 was determined in hippocampus tissues via reverse transcription-quantitative PCR and western blotting, respectively. Compared with normal mice, rats with AD had significantly decreased learning abilities, increased cell apoptosis rates, increased levels of AChE, iNOS, ROS, MDA, MAPK1 and p-MAPK1 and decreased levels of SOD, GSH-Px and miR-132. Upregulation of miR-132 group improved the above indictors and silencing MAKP1 worsened the condition of rats. miR-132 upregulation therefore reversed the negative effects caused by MAPK1 silencing in rats with AD. In conclusion, miR-132 inhibited hippocampal iNOS expression and oxidative stress by inhibiting MAPK1expression to improve the cognitive function of rats with AD.
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