ReviewMovement disorders : official journal of the Movement Disorder Society2019
The usual suspects, dopamine and alpha-synuclein, conspire to cause neurodegeneration.
Review in Movement disorders : official journal of the Movement Disorder Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 108 citations in OpenAlex.
- Expanding the DAD9-Pegasus Scaffold: Synthesis and Functional Evaluation of Sulfur-Containing Dopamine-Tetracycline Conjugates for Parkinson's Disease.ChemMedChem · 2026Article
- Dopamine Abundance Uncouples Neurodegeneration and Lifespan in abioRxiv : the preprint server for biology · 2026Article
- Soluble α-synuclein oligomers drive transient corticostriatal pathology and delayed nigral vulnerability in a mouse model of early α-synucleinopathy.Acta neuropathologica communications · 2026Article
- The Influence of Gut Microbiome on Alpha-Synuclein Aggregation: Implications for Parkinson's Disease Pathogenesis.Molecular neurobiology · 2026Review
- From Neuroadaptation to Neuroprogression: Rethinking Chronic Cocaine Exposure Through a Model of Cocaine-Related Cerebropathy.Journal of clinical medicine · 2026Article
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Autonomic dysfunction in neurodegenerative disease.Nature reviews. Neuroscience · 2025Review
- Potential therapeutic effects of curcumin, with or without L-DOPA, on motor and cognitive functions and hippocampal changes in rotenone-treated rats.Metabolic brain disease · 2025Article
- Non-enzymatic posttranslational protein modifications in protein aggregation and neurodegenerative diseases.RSC chemical biology · 2025Review
- Manganese exposure induces parkinsonism-like symptoms by Serpina3n-TFEB-v/p-ATPase signaling mediated lysosomal dysfunction.Cell biology and toxicology · 2025Article
- Decoding crosstalk between neurotransmitters and α-synuclein in Parkinson's disease: pathogenesis and therapeutic implications.Therapeutic advances in neurological disorders · 2025Review
- Small Molecules, α-Synuclein Pathology, and the Search for Effective Treatments in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Targets to Search for New Pharmacological Treatment in Idiopathic Parkinson's Disease According to the Single-Neuron Degeneration Model.Biomolecules · 2024Review
- Gut microbiome, short-chain fatty acids, alpha-synuclein, neuroinflammation, and ROS/RNS: Relevance to Parkinson's disease and therapeutic implications.Redox biology · 2024Review
- Exploring Caenorhabditis elegans as Parkinson's Disease Model: Neurotoxins and Genetic Implications.Neurotoxicity research · 2024Review
- Impaired cerebral microvascular endothelial cells integrity due to elevated dopamine in myasthenic model.Journal of neuroinflammation · 2024Article
- Dysbiosis of the gut microbiota and its effect on α-synuclein and prion protein misfolding: consequences for neurodegeneration.Frontiers in cellular and infection microbiology · 2024Review
- Non-invasive systemic viral delivery of human alpha-synuclein mimics selective and progressive neuropathology of Parkinson's disease in rodent brains.Molecular neurodegeneration · 2023Article
- Role of dopamine in the pathophysiology of Parkinson's disease.Translational neurodegeneration · 2023Review
- Development of Small Molecules Targeting α-Synuclein Aggregation: A Promising Strategy to Treat Parkinson's Disease.Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is primarily a movement disorder driven by the loss of dopamine-producing neurons in the substantia nigra (SN). Early identification of the oxidative properties of dopamine implicated it as a potential source of oxidative stress in PD, yet few studies have investigated dopamine neurotoxicity in vivo. The discovery of PD-causing mutations in α-synuclein and the presence of aggregated α-synuclein in the hallmark Lewy body pathology of PD revealed another important player. Despite extensive efforts, the precise role of α-synuclein aggregation in neurodegeneration remains unclear. We recently manipulated both dopamine levels and α-synuclein expression in aged mice and found that only the combination of these 2 factors caused progressive neurodegeneration of the SN and an associated motor deficit. Dopamine modified α-synuclein aggregation in the SN, resulting in greater abundance of α-synuclein oligomers and unique dopamine-induced oligomeric conformations. Furthermore, disruption of the dopamine-α-synuclein interaction rescued dopaminergic neurons from degeneration in transgenic Caenorhabditis elegans models. In this Perspective, we discuss these findings in the context of known α-synuclein and dopamine biology, review the evidence for α-synuclein oligomer toxicity and potential mechanisms, and discuss therapeutic implications. © 2019 International Parkinson and Movement Disorder Society.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.