ReviewBiomolecules2015
Interaction between Neuromelanin and Alpha-Synuclein in Parkinson's Disease.
Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The trial behind it
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Who cites it
26 citing papers in PubMed.
- A Pathophysiological Model of Parkinson's Disease Based on Microvascular Flow Disturbance and Leukocyte-Mediated Oxidative Injury in Critical Pigmented Neuronal Niches.Antioxidants (Basel, Switzerland) · 2026Article
- Radiation-Induced Neurodegeneration.Biomedicines · 2026Review
- Revisiting the alpha-synuclein paradox in melanoma-Parkinson's disease connection: more than a tale of two cell fates.Cellular and molecular life sciences : CMLS · 2025Review
- Induction of Ferroptotic Cell Death by Neuromelanin Pigments in Dopaminergic Cells.ACS chemical neuroscience · 2025Article
- The α-Synuclein Seeding Amplification Assay for Parkinson's Disease.International journal of molecular sciences · 2025Review
- Link between Parkinson's disease and melanoma: insights into the influence of theFrontiers in oncology · 2025Review
- New Aspects Regarding the Fluorescence Spectra of Melanin and Neuromelanin in Pigmented Human Tissue Concerning Hypoxia.International journal of molecular sciences · 2024Article
- Catecholamines and Parkinson's disease: tyrosine hydroxylase (TH) over tetrahydrobiopterin (BH4) and GTP cyclohydrolase I (GCH1) to cytokines, neuromelanin, and gene therapy: a historical overview.Journal of neural transmission (Vienna, Austria : 1996) · 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
- New hope for Parkinson's disease treatment: Targeting gut microbiota.CNS neuroscience & therapeutics · 2022Review
- Lafora Disease and Alpha-Synucleinopathy in Two Adult Free-Ranging Moose (Animals : an open access journal from MDPI · 2022Article
- α-Synuclein phosphorylation at serine 129 occurs after initial protein deposition and inhibits seeded fibril formation and toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neuromelanin in Parkinson's Disease: Tyrosine Hydroxylase and Tyrosinase.International journal of molecular sciences · 2022Review
- Examining the Toxicity of α-Synuclein in Neurodegenerative Disorders.Life (Basel, Switzerland) · 2021Review
- Production, purification, and characterization of Streptomyces sp. strain MPPS2 extracellular pyomelanin pigment.Archives of microbiology · 2021Article
- Changes in cytoplasmic and extracellular neuromelanin in human substantia nigra with normal aging.European journal of histochemistry : EJH · 2021Article
- Rasagiline and selegiline modulate mitochondrial homeostasis, intervene apoptosis system and mitigate α-synuclein cytotoxicity in disease-modifying therapy for Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Association Between Parkinson's Disease and Melanoma: Putting the Pieces Together.Frontiers in aging neuroscience · 2020Article
- Selective Neuronal Death in Neurodegenerative Diseases: The Ongoing Mystery.The Yale journal of biology and medicine · 2019Review
- α-Synuclein in Parkinson's disease: causal or bystander?Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn.
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Registered trials
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