ArticleNature neuroscience2017
Dopamine induces soluble α-synuclein oligomers and nigrostriatal degeneration.
Article in Nature neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 220 citations in OpenAlex.
- Nigrostriatal dopaminergic vulnerability in Parkinson's disease: Neuroprotective strategies.Neural regeneration research · 2026Article
- 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
- Polymeric lysosome-targeting chimeras for extracellular α-synuclein degradation in Parkinson's disease.Acta neuropathologica communications · 2026Review
- Mouse model of atypical DAT deficiency syndrome uncovers dopamine dysfunction associated with parkinsonism and ADHD.The Journal of clinical investigation · 2026Article
- VMAT2 dysfunction impairs vesicular dopamine uptake, driving its oxidation and α-synuclein pathology in DJ-1-linked Parkinson's neurons.Science advances · 2026Article
- Pyridoxamine inhibits dopamine-induced α-synuclein oligomerization through scavenging neurotoxic dopamine quinone.Scientific reports · 2025Article
- Leveraging open cheminformatics tools for non-targeted metabolomics analysis of C. elegans: a workflow comparison and application to strains related to xenobiotic metabolism and neurodegeneration.Analytical and bioanalytical chemistry · 2025Article
- Pathogenic mechanism underlying parkinsonism induced by neurotoxicants (MPTP and 6-hydroxydopamine) and α-synuclein: a unifying hypothesis.Journal of molecular cell biology · 2025Review
- Nanoplasmonic Infrared Microarray Sensor Enabling Structural Protein Biomarker-Based Drug Screening for Neurodegenerative Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cerebrospinal fluid draining lymphatics in health and disease: advances and controversies.Nature cardiovascular research · 2025Review
- The Neurotoxic Properties of α-synuclein Polymorphs.Experimental neurobiology · 2025Article
- Correlations Between Amelioration of Rotenone-Induced Parkinson's Symptoms byInternational journal of molecular sciences · 2025Article
- The α-Synuclein Seeding Amplification Assay for Parkinson's Disease.International journal of molecular sciences · 2025Review
- Decoding crosstalk between neurotransmitters and α-synuclein in Parkinson's disease: pathogenesis and therapeutic implications.Therapeutic advances in neurological disorders · 2025Review
- Longitudinal neuromelanin changes in prodromal and early Parkinson's disease in humans and rat model.Brain communications · 2025Article
- Small Molecules, α-Synuclein Pathology, and the Search for Effective Treatments in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Modelling human neuronal catecholaminergic pigmentation in rodents recapitulates age-related neurodegenerative deficits.Nature communications · 2024Article
- Histamine synthesis and transport are coupled in axon terminals via a dual quality control system.The EMBO journal · 2024Article
- The protective effects of repetitive transcranial magnetic stimulation with different high frequencies on motor functions in MPTP/probenecid induced Parkinsonism mouse models.Brain and behavior · 2024Article
73 more citing papers are in PubMed but not listed here.
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15 authors at 7 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is defined by the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy body inclusions containing aggregated α-synuclein. Efforts to explain dopamine neuron vulnerability are hindered by the lack of dopaminergic cell death in α-synuclein transgenic mice. To address this, we manipulated both dopamine levels and α-synuclein expression. Nigrally targeted expression of mutant tyrosine hydroxylase with enhanced catalytic activity increased dopamine levels without damaging neurons in non-transgenic mice. In contrast, raising dopamine levels in mice expressing human A53T mutant α-synuclein induced progressive nigrostriatal degeneration and reduced locomotion. Dopamine elevation in A53T mice increased levels of potentially toxic α-synuclein oligomers, resulting in conformationally and functionally modified species. Moreover, in genetically tractable Caenorhabditis elegans models, expression of α-synuclein mutated at the site of interaction with dopamine prevented dopamine-induced toxicity. These data suggest that a unique mechanism links two cardinal features of PD: dopaminergic cell death and α-synuclein aggregation.
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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.