ReviewCells2021
The Nigral Coup in Parkinson's Disease by α-Synuclein and Its Associated Rebels.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Research Progress on the Mechanism of Ginsenosides in the Treatment of Parkinson's Disease.International journal of molecular sciences · 2026Review
- Salidroside Protects Against Simazine-Induced Neurotoxicity by ActivatingInternational journal of molecular sciences · 2026Article
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- The brain and heart-axis in neurodegeneration and cardiovascular disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- The lifespan continuum of brain disorders: investigating links between neurodevelopmental and neurodegenerative disease-chicken or egg?Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Inflammation as common link to progressive neurological diseases.Archives of toxicology · 2024Review
- Identification of the bacterial metabolite aerugine as potential trigger of human dopaminergic neurodegeneration.Environment international · 2023Article
- Lewy bodies, iron, inflammation and neuromelanin: pathological aspects underlying Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Neurodegenerative Diseases: Can Caffeine Be a Powerful Ally to Weaken Neuroinflammation?International journal of molecular sciences · 2022Review
- A brief history of brain iron accumulation in Parkinson disease and related disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Neuromelanin in Parkinson's Disease: Tyrosine Hydroxylase and Tyrosinase.International journal of molecular sciences · 2022Review
- Propolis induces cardiac metabolism changes in 6-hydroxydopamine animal model: A dietary intervention as a potential cardioprotective approach in Parkinson's disease.Frontiers in pharmacology · 2022Article
- Iron as the concert master in the pathogenic orchestra playing in sporadic Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Possible Link between SARS-CoV-2 Infection and Parkinson's Disease: The Role of Toll-Like Receptor 4.International journal of molecular sciences · 2021Review
- Review
- Simultaneous treatment with cells and rosemary extract ameliorates 6-OHDA-induced toxicity in the hippocampus of mice.Journal of advanced pharmaceutical technology & researchArticle
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
The risk of Parkinson's disease increases with age. However, the etiology of the illness remains obscure. It appears highly likely that the neurodegenerative processes involve an array of elements that influence each other. In addition, genetic, endogenous, or exogenous toxins need to be considered as viable partners to the cellular degeneration. There is compelling evidence that indicate the key involvement of modified α-synuclein (Lewy bodies) at the very core of the pathogenesis of the disease. The accumulation of misfolded α-synuclein may be a consequence of some genetic defect or/and a failure of the protein clearance system. Importantly, α-synuclein pathology appears to be a common denominator for many cellular deleterious events such as oxidative stress, mitochondrial dysfunction, dopamine synaptic dysregulation, iron dyshomeostasis, and neuroinflammation. These factors probably employ a common apoptotic/or autophagic route in the final stages to execute cell death. The misfolded α-synuclein inclusions skillfully trigger or navigate these processes and thus amplify the dopamine neuron fatalities. Although the process of neuroinflammation may represent a secondary event, nevertheless, it executes a fundamental role in neurodegeneration. Some viral infections produce parkinsonism and exhibit similar characteristic neuropathological changes such as a modest brain dopamine deficit and α-synuclein pathology. Thus, viral infections may heighten the risk of developing PD. Alternatively, α-synuclein pathology may induce a dysfunctional immune system. Thus, sporadic Parkinson's disease is caused by multifactorial trigger factors and metabolic disturbances, which need to be considered for the development of potential drugs in the disorder.
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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 Socratic graph.