ArticleProceedings of the National Academy of Sciences of the United States of America2002
Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers, 1 of them a synthesis that pooled it.
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Who cites it
243 citing papers in PubMed, 1 synthesis or guideline pooled it, 574 citations in OpenAlex.
- Pre-clinical Studies Identifying Molecular Pathways of Neuroinflammation in Parkinson's Disease: A Systematic Review.Frontiers in aging neuroscience · 2022Pooled it
- α-Synuclein expression is required for somatodendritic dopamine release and immediate early gene induction.Science advances · 2026Article
- Synphilin-1 modulates alpha-synuclein assembly, release and uptake.NPJ Parkinson's disease · 2025Article
- Exploring α-Syn's Functions Through Ablation Models: Physiological and Pathological Implications.Cellular and molecular neurobiology · 2025Review
- ZSCAN21 mediates the pathogenic transcriptional induction of α-synuclein in cellular and animal models of Parkinson's disease.Cell death & disease · 2025Article
- Loss of Nocturnin increases neuronal viability in oxidative stress conditions.Frontiers in neuroscience · 2025Article
- Alpha-synuclein null mutation exacerbates the phenotype of a model of Menkes disease in female mice.Frontiers in neuroscience · 2025Article
- Decoding crosstalk between neurotransmitters and α-synuclein in Parkinson's disease: pathogenesis and therapeutic implications.Therapeutic advances in neurological disorders · 2025Review
- Mitochondrial dysfunction in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Malvidin-3-O-Glucoside Mitigates α-Syn and MPTP Co-Induced Oxidative Stress and Apoptosis in Human Microglial HMC3 Cells.International journal of molecular sciences · 2024Article
- A novel function for α-synuclein as a regulator of NCK2 in olfactory bulb: implications for its role in olfaction.Cell & bioscience · 2024Article
- Construct, Face, and Predictive Validity of Parkinson's Disease Rodent Models.International journal of molecular sciences · 2024Review
- Retinal hyperspectral imaging in mouse models of Parkinson's disease and healthy aging.Scientific reports · 2024Article
- Neurotoxicology of dopamine: Victim or assailant?Neurotoxicology · 2024Review
- Alpha-Synuclein Gene Alterations Modulate Tyrosine Hydroxylase in Human iPSC-Derived Neurons in a Parkinson's Disease Animal Model.Life (Basel, Switzerland) · 2024Article
- ENGINEERED NANOBODIES WITH PROGRAMMABLE TARGET ANTIGEN PROTEOLYSIS (PTAP) FUSIONS REGULATE INTRACELLULAR ALPHA-SYNUCLEIN IN VITRO AND IN VIVO.Research square · 2024Article
- Neuropathogenesis-on-chips for neurodegenerative diseases.Nature communications · 2024Review
- Recalibrating the Why and Whom of Animal Models in Parkinson Disease: A Clinician's Perspective.Brain sciences · 2024Review
- RETRACTED: Vitamin E Analog Trolox Attenuates MPTP-Induced Parkinson's Disease in Mice, Mitigating Oxidative Stress, Neuroinflammation, and Motor Impairment.International journal of molecular sciences · 2023Article
- α-Synuclein in synaptic function and dysfunction.Trends in neurosciences · 2023Review
183 more citing papers are in PubMed but not listed here.
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17 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is most commonly a sporadic illness, and is characterized by degeneration of substantia nigra dopamine (DA) neurons and abnormal cytoplasmic aggregates of alpha-synuclein. Rarely, PD may be caused by missense mutations in alpha-synuclein. MPTP, a neurotoxin that inhibits mitochondrial complex I, is a prototype for an environmental cause of PD because it produces a pattern of DA neurodegeneration that closely resembles the neuropathology of PD. Here we show that alpha-synuclein null mice display striking resistance to MPTP-induced degeneration of DA neurons and DA release, and this resistance appears to result from an inability of the toxin to inhibit complex I. Contrary to predictions from in vitro data, this resistance is not due to abnormalities of the DA transporter, which appears to function normally in alpha-synuclein null mice. Our results suggest that some genetic and environmental factors that increase susceptibility to PD may interact with a common molecular pathway, and represent the first demonstration that normal alpha-synuclein function may be important to DA neuron viability.
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