ArticleMolecular therapy. Nucleic acids2022
Modulation of miR-181 influences dopaminergic neuronal degeneration in a mouse model of Parkinson's disease.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- The Diagnostic and Therapeutic Value of Micro-RNA in Parkinson's Disease.Cellular and molecular neurobiology · 2026Review
- MicroRNA-181 influences Alzheimer's risk by regulating neprilysin and microtubule-associated tau pathways, offering a novel target.bioRxiv : the preprint server for biology · 2026Article
- Downregulation of miRNAs Accompanies Increased HERV-K (HML-2) Expression in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2026Article
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- Non-coding RNAs in Parkinson's Disease: Pathogenesis, Exosomes, and Therapeutic Horizons.Cellular and molecular neurobiology · 2025Review
- MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025Review
- Targeted miRNA Delivery in Epilepsy: Mechanisms, Advances, and Therapeutic Potential.Molecular biology reports · 2025Review
- Mitochondrial microRNAs (mitomiRs) as emerging biomarkers and therapeutic targets for chronic human diseases.Frontiers in genetics · 2025Review
- MicroRNAs Fine-Tune Brain and Body Communication in Health and Disease : MicroRNAs in Brain-Body Communication.Advances in experimental medicine and biology · 2025Review
- The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer's and Parkinson's Diseases.Cellular and molecular neurobiology · 2024Review
- Review
- Mitochondria-Associated MicroRNAs and Parkinson's Disease.Neuroscience insights · 2024Review
- Modulation of miR-29 influences myocardial compliance likely through coordinated regulation of calcium handling and extracellular matrix.Molecular therapy. Nucleic acids · 2023Article
- Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- Clinical Trials of Non-Coding RNAs as Diagnostic and Therapeutic Biomarkers for Central Nervous System Injuries.Current neuropharmacology · 2023Article
- Neuronal dysfunction and gene modulation by non-coding RNA in Parkinson's disease and synucleinopathies.Frontiers in cellular neuroscience · 2023Review
- Understanding the Involvement of microRNAs in Mitochondrial Dysfunction and Their Role as Potential Biomarkers and Therapeutic Targets in Parkinson's Disease.Journal of Alzheimer's disease : JAD · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is caused by the loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although PD pathogenesis is not fully understood, studies implicate perturbations in gene regulation, mitochondrial function, and neuronal activity. MicroRNAs (miRs) are small gene regulatory RNAs that inhibit diverse subsets of target mRNAs, and several studies have noted miR expression alterations in PD brains. For example, miR-181a is abundant in the brain and is increased in PD patient brain samples; however, the disease relevance of this remains unclear. Here, we show that miR-181 target mRNAs are broadly downregulated in aging and PD brains. To address whether the miR-181 family plays a role in PD pathogenesis, we generated adeno-associated viruses (AAVs) to overexpress and inhibit the miR-181 isoforms. After co-injection with AAV overexpressing alpha-synuclein (aSyn) into mouse SN (PD model), we found that moderate miR-181a/b overexpression exacerbated aSyn-induced DA neuronal loss, whereas miR-181 inhibition was neuroprotective relative to controls (GFP alone and/or scrambled RNA). Also, prolonged miR-181 overexpression in SN alone elicited measurable neurotoxicity that is coincident with an increased immune response. mRNA-seq analyses revealed that miR-181a/b inhibits genes involved in synaptic transmission, neurite outgrowth, and mitochondrial respiration, along with several genes having known protective roles and genetic links in PD.
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Registered trials
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