ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
The parkinsonian mimetic, MPP+, specifically impairs mitochondrial transport in dopamine axons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 130 citations in OpenAlex.
- 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
- Neuronal mitochondrial dynamics: roles in brain disorders and therapeutic potential.Acta pharmacologica Sinica · 2026Article
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Calpain-2 Regulates Kinesin and Dynein Dysfunction in Neurotoxin-Induced Motoneuron Injury.Brain sciences · 2026Article
- Scattering approach to diffusion quantifies axonal damage in brain injury.Nature communications · 2025Article
- Article
- White matter lesions contribute to motor and non-motor disorders in Parkinson's disease: a critical review.GeroScience · 2025Review
- Neuroprotective Agents: Implications for Parkinson's Disease Treatment.Current Alzheimer research · 2025Review
- Initial Molecular Mechanisms of the Pathogenesis of Parkinson's Disease in a Mouse Neurotoxic Model of the Earliest Preclinical Stage of This Disease.International journal of molecular sciences · 2024Article
- Linking acetylated α-Tubulin redistribution to α-Synuclein pathology in brain of Parkinson's disease patients.NPJ Parkinson's disease · 2024Article
- Acetylated α-Tubulin and α-Synuclein: Physiological Interplay and Contribution to α-Synuclein Oligomerization.International journal of molecular sciences · 2023Article
- Circulating (Poly)phenol Metabolites: Neuroprotection in a 3D Cell Model of Parkinson's Disease.Molecular nutrition & food research · 2022Article
- Bacopa Protects against Neurotoxicity Induced by MPPMolecules (Basel, Switzerland) · 2022Article
- Synapses: The Brain's Energy-Demanding Sites.International journal of molecular sciences · 2022Review
- Autophagy-dependent removal of α-synuclein: a novel mechanism of GM1 ganglioside neuroprotection against Parkinson's disease.Acta pharmacologica Sinica · 2021Article
- Mitochondrial Quality Control Strategies: Potential Therapeutic Targets for Neurodegenerative Diseases?Frontiers in neuroscience · 2021Review
- Calcium, Bioenergetics, and Parkinson's Disease.Cells · 2020Review
- Analyzing Mitochondrial Transport and Morphology in Human Induced Pluripotent Stem Cell-Derived Neurons in Hereditary Spastic Paraplegia.Journal of visualized experiments : JoVE · 2020Article
- Neurorestorative Effects of a Novel Fas-Associated Factor 1 Inhibitor in the MPTP Model: An [Frontiers in pharmacology · 2020Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Impaired axonal transport may play a key role in Parkinson's disease. To test this notion, a microchamber system was adapted to segregate axons from cell bodies using green fluorescent protein-labeled mouse dopamine (DA) neurons. Transport was examined in axons challenged with the DA neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+). MPP+ rapidly reduced overall mitochondrial motility in DA axons; among motile mitochondria, anterograde transport was slower yet retrograde transport was increased. Transport effects were specific for DA mitochondria, which were smaller and transported more slowly than their non-DA counterparts. MPP+ did not affect synaptophysin-tagged vesicles or any other measureable moving particle. Toxin effects on DA mitochondria were not dependent upon ATP, calcium, free radical species, JNK, or caspase3/PKC pathways but were completely blocked by the thiol-anti-oxidant N-acetyl-cysteine or membrane-permeable glutathione. Since these drugs also rescued processes from degeneration, these findings emphasize the need to develop therapeutics aimed at axons as well as cell bodies to preserve "normal" circuitry and function as long as possible.
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Registered trials
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