ReviewJournal of neural transmission (Vienna, Austria : 1996)2020
The role of alpha-synuclein as ferrireductase in neurodegeneration associated with Parkinson's disease.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- Nanomaterial-based approaches to neurotoxin neutralization in neurodegenerative diseases.Nanomedicine (London, England) · 2025Review
- The interplay of iron, oxidative stress, and α-synuclein in Parkinson's disease progression.Molecular medicine (Cambridge, Mass.) · 2025Review
- Emerging Ferroptosis Involvement in Amyotrophic Lateral Sclerosis Pathogenesis: Neuroprotective Activity of Polyphenols.Molecules (Basel, Switzerland) · 2025Review
- Flexible iron: disorder in the ironome brings order to protein structure and function.Frontiers in molecular biosciences · 2025Article
- Iron Metabolism and Ferroptosis in Early Brain Injury after Subarachnoid Haemorrhage.Molecular neurobiology · 2024Review
- The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
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- Lewy bodies, iron, inflammation and neuromelanin: pathological aspects underlying Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Role and mechanism of ferroptosis in neurological diseases.Molecular metabolism · 2022Review
- Empirical evidence for biometal dysregulation in Parkinson's disease from a systematic review and Bradford Hill analysis.NPJ Parkinson's disease · 2022Review
- Neonatal 6-hydroxydopamine lesioning of rats and dopaminergic neurotoxicity: proposed animal model of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Toxic Feedback Loop Involving Iron, Reactive Oxygen Species, α-Synuclein and Neuromelanin in Parkinson's Disease and Intervention with Turmeric.Molecular neurobiology · 2021Review
- Iron as the concert master in the pathogenic orchestra playing in sporadic Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Review
- Review
- Experimental Dopamine Reuptake Inhibitors in Parkinson's Disease: A Review of the Evidence.Journal of experimental pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Misfolding of the protein α-synuclein contributes to the formation of the intracellular inclusion, Lewy bodies. Although these structures are not exclusive to Parkinson's disease, nevertheless, their presence in the substantia nigra is mandatory for the pathological diagnosis of the disorder. Therefore, there must be a focus on the pathological mechanisms responsible for Lewy body generation. Recent studies have suggested that α-synuclein has the potential to operate as the enzyme ferrireductase. Perhaps in the early diseased state, overexpression or mutation of alpha-synuclein/ferrireductase invokes the dyshomeostasis of iron (III)/(II) only, while in advanced stages, accumulation of iron in particular areas of the brain follows. Furthermore, the loss of an important iron chelator, neuromelanin (due to dopaminergic neuronal death), may then result in the release and increase in unbound free iron. Iron could generate reactive oxygen species, which could instigate a torrent of cellular deleterious processes. In addition, loss of energy supply may contribute to the alteration in activity of enzymes involved in the mitochondrial respiratory chain and would, therefore, confer a vulnerability to the dopaminergic neurons in the substantia nigra. Therefore, the ferrireductase alpha-synuclein may hold the key for major pathology of Parkinson's disease. In conclusion, we hypothesize that environmentally or genetically overexpressed and/or mutated α-synuclein/ferrireductase causes iron dyshomeostasis without increase of free iron concentration in the early phases of PD, while increased iron concentration accompanied by iron dyshomeostasis is a marker for progressed PD stages. It is essential to elucidate these degenerative mechanisms, so as to provide effective therapeutic treatment to halt or delay the progression of the illness already in the early phase of PD. The development of iron chelators seems to be a reasonable approach.
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