ArticleJournal of neural transmission (Vienna, Austria : 1996)2012
Neuromelanin enhances the toxicity of α-synuclein in SK-N-SH cells.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Neuromelanin-induced cellular stress and neurotoxicity in the pathogenesis of Parkinson's disease.Apoptosis : an international journal on programmed cell death · 2025Review
- The α-Synuclein Seeding Amplification Assay for Parkinson's Disease.International journal of molecular sciences · 2025Review
- Targeting Ferroptosis in Parkinson's Disease: Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Antioxidant, neuroprotective, and neuroblastoma cells (SH-SY5Y) differentiation effects of melanins and arginine-modified melanins from Daedaleopsis tricolor and Fomes fomentarius.BMC biotechnology · 2024Article
- Selective dopaminergic neurotoxicity modulated by inherent cell-type specific neurobiology.Neurotoxicology · 2024Review
- Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Role of dopamine in the pathophysiology of Parkinson's disease.Translational neurodegeneration · 2023Review
- Assessment of Neuroprotective Effects of Low-Intensity Transcranial Ultrasound Stimulation in a Parkinson's Disease Rat Model by Fractional Anisotropy and Relaxation Time T2Frontiers in neuroscience · 2021Article
- α-Synuclein in Parkinson's disease: causal or bystander?Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Mobility Deficits Assessed With Mobile Technology: What Can We Learn From Brain Iron-Altered Animal Models?Frontiers in neurology · 2019Review
- Overexpression of alpha-synuclein at non-toxic levels increases dopaminergic cell death induced by copper exposure via modulation of protein degradation pathways.Neurobiology of disease · 2015Article
- Melanin affinity and its possible role in neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2013Review
- The role of oxidative stress in Parkinson's disease.Journal of Parkinson's disease · 2013Review
- The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells.PloS one · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The key pathological feature of Parkinson's disease (PD) is selective degeneration of the neuromelanin (NM)-pigmented dopaminergic neurons in the substantia nigra (SN). NM, like other risk factors, such as oxidative stress (OS) and α-synuclein (α-syn), is involved in the pathogenesis of PD. But whether or not NM synergizes with α-syn or OS in the pathogenesis of PD remains unexplored. In the present study, we examined the effects of NM on cellular viability, apoptosis and free radical production in α-syn over-expressing human neuroblastoma cell line (SK-N-SH) in the presence or absence of the oxidizer Fenton's Reagent (FR). We showed that NM synergized with FR in suppressing cell viability, and in inducing apoptosis and hydroxyl radical production in all SK-N-SH cell lines. α-Syn over-expressing cells exhibited more pronounced effect, especially the A53T mutation. Our findings suggest that NM synergizes with both OS and α-syn in conferring dopaminergic vulnerability, adding to our understanding of the pathogenesis of PD.
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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.