ArticleScientific reports2017
DOPAL derived alpha-synuclein oligomers impair synaptic vesicles physiological function.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed.
- Catecholamine metabolism revisited: from neurochemistry to integrative physiology and pathophysiology.Physiological reviews · 2026Review
- Development of 1-(substituted benzofuran-2-yl)-3-(halogen-substituted phenyl)prop-2-en-1-ones as potent, reversible, and selective MAO-B inhibitors for Parkinson's Disease.Scientific reports · 2026Article
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- ALH Inhibition as a Molecular Initiating Event in the Adverse Outcome Pathway of Benomyl Toxicity inInternational journal of molecular sciences · 2025Article
- Ferroptosis: a new target for depression prevention and treatment.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Article
- CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson's disease models.Journal of neuroinflammation · 2025Article
- Reversing Signs of Parkinsonism in a Cell Model Using Mitochondria-Targeted Organoiridium Catalysis.Journal of medicinal chemistry · 2025Article
- Decoding crosstalk between neurotransmitters and α-synuclein in Parkinson's disease: pathogenesis and therapeutic implications.Therapeutic advances in neurological disorders · 2025Review
- Evolutionary conservation of dopamine-mediated cellular plasticity in Arctic sponges (Porifera).Frontiers in molecular biosciences · 2025Article
- Ferroptosis-A Shared Mechanism for Parkinson's Disease and Type 2 Diabetes.International journal of molecular sciences · 2024Review
- Rethinking Parkinson's disease: could dopamine reduction therapy have clinical utility?Journal of neurology · 2024Review
- Selective dopaminergic neurotoxicity modulated by inherent cell-type specific neurobiology.Neurotoxicology · 2024Review
- Neurotoxicology of dopamine: Victim or assailant?Neurotoxicology · 2024Review
- Sequestosome-1 (SQSTM1/p62) as a target in dopamine catabolite-mediated cellular dyshomeostasis.Cell death & disease · 2024Article
- Key genes and convergent pathogenic mechanisms in Parkinson disease.Nature reviews. Neuroscience · 2024Review
- Disruption of Dopamine Homeostasis Associated with Alteration of Proteins in Synaptic Vesicles: A Putative Central Mechanism of Parkinson's Disease Pathogenesis.Aging and disease · 2024Review
- Transcriptomic profiling of early synucleinopathy in rats induced with preformed fibrils.NPJ Parkinson's disease · 2024Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors.
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Abstract
Parkinson's disease is a neurodegenerative disorder characterized by the death of dopaminergic neurons and by accumulation of alpha-synuclein (aS) aggregates in the surviving neurons. The dopamine catabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL) is a highly reactive and toxic molecule that leads to aS oligomerization by covalent modifications to lysine residues. Here we show that DOPAL-induced aS oligomer formation in neurons is associated with damage of synaptic vesicles, and with alterations in the synaptic vesicles pools. To investigate the molecular mechanism that leads to synaptic impairment, we first aimed to characterize the biochemical and biophysical properties of the aS-DOPAL oligomers; heterogeneous ensembles of macromolecules able to permeabilise cholesterol-containing lipid membranes. aS-DOPAL oligomers can induce dopamine leak in an in vitro model of synaptic vesicles and in cellular models. The dopamine released, after conversion to DOPAL in the cytoplasm, could trigger a noxious cycle that further fuels the formation of aS-DOPAL oligomers, inducing neurodegeneration.
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