ArticleMolecular neurodegeneration2014
The Parkinsonian mimetic, 6-OHDA, impairs axonal transport in dopaminergic axons.
Article in Molecular neurodegeneration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- The irony of Parkinson's disease: Converging mechanisms of redox imbalance and ferroptosis.Redox biology · 2026Review
- Expression of Axonal Transport Proteins in Dopaminergic Neurons of the Substantia Nigra in Mouse Models of Preclinical and Clinical Stages of Parkinson's Disease.International journal of molecular sciences · 2026Article
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Temporal assessment of behavior in Parkinson's visual hallucinations via a multidimensional analysis strategy.Signal transduction and targeted therapy · 2026Article
- Multi-Omics Analysis Reveals Distinct Lipid Remodelling and Mitochondrial Stress in SH-SY5Y Cells Modelling Parkinson's Disease.Metabolites · 2025Article
- Mode of Action of Toxin 6-Hydroxydopamine in SH-SY5Y Using NMR Metabolomics.Molecules (Basel, Switzerland) · 2025Article
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- Ideal animal models according to multifaceted mechanisms and peculiarities in neurological disorders: present and challenges.Archives of pharmacal research · 2025Review
- Evaluating the Role of Lin-11, Isl-1, and Mec-3 Kinases in Dopaminergic Neurodegeneration in a Subacute 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Parkinson's Disease.ACS pharmacology & translational science · 2024Article
- IRE1/JNK Is the Leading UPR Pathway in 6-OHDA-Induced Degeneration of Differentiated SH-SY5Y Cells.International journal of molecular sciences · 2024Article
- Bioactive components, pharmacological properties and underlying mechanism ofChinese herbal medicines · 2024Review
- Ergothioneine-Mediated Neuroprotection of Human iPSC-Derived Dopaminergic Neurons.Antioxidants (Basel, Switzerland) · 2024Article
- Extracellular Vesicles: A New Approach to Study the Brain's Neural System and Its Diseases.Cell biochemistry and biophysics · 2024Review
- Research Progress on the Experimental Model and Underlying Mechanistic Studies of Tension-Type Headaches.Current pain and headache reports · 2024Review
- DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Human neural stem cell-derived extracellular vesicles protect against Parkinson's disease pathologies.Journal of nanobiotechnology · 2022Article
- Dopaminergic Axons: Key Recitalists in Parkinson's Disease.Neurochemical research · 2022Review
- Perivascular Adipose Tissue Anticontractile Function Is Mediated by Both Endothelial and Neuronal Nitric Oxide Synthase Isoforms.Journal of vascular research · 2022Article
- Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- Transgenic Mice Expressing Human α-Synuclein 1-103 Fragment as a Novel Model of Parkinson's Disease.Frontiers in aging neuroscience · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
6-hydroxydopamine (6-OHDA) is one of the most commonly used toxins for modeling degeneration of dopaminergic (DA) neurons in Parkinson's disease. 6-OHDA also causes axonal degeneration, a process that appears to precede the death of DA neurons. To understand the processes involved in 6-OHDA-mediated axonal degeneration, a microdevice designed to isolate axons fluidically from cell bodies was used in conjunction with green fluorescent protein (GFP)-labeled DA neurons. Results showed that 6-OHDA quickly induced mitochondrial transport dysfunction in both DA and non-DA axons. This appeared to be a general effect on transport function since 6-OHDA also disrupted transport of synaptophysin-tagged vesicles. The effects of 6-OHDA on mitochondrial transport were blocked by the addition of the SOD1-mimetic, Mn(III)tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), as well as the anti-oxidant N-acetyl-cysteine (NAC) suggesting that free radical species played a role in this process. Temporally, microtubule disruption and autophagy occurred after transport dysfunction yet before DA cell death following 6-OHDA treatment. The results from the study suggest that ROS-mediated transport dysfunction occurs early and plays a significant role in inducing axonal degeneration in response to 6-OHDA treatment.
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