ReviewJournal of neural transmission (Vienna, Austria : 1996)2019
α-Synuclein in Parkinson's disease: causal or bystander?
Review in Journal of neural transmission (Vienna, Austria : 1996), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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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.
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Who cites it
70 citing papers in PubMed, 112 citations in OpenAlex.
- Considerations for therapeutic targets for clinical trials in biomarker-characterized prodromal Parkinson's disease populations.Journal of Parkinson's disease · 2026Article
- Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.Neuromolecular medicine · 2026Review
- The Influence of Gut Microbiome on Alpha-Synuclein Aggregation: Implications for Parkinson's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- A Novel 3D Semi-Automated Full Quantification Technique for Detection of Intraneural Phospho-α-Synuclein in Skin Biopsies.European journal of neurology · 2026Article
- The potential role of adenosinergic pathway and methylxanthines in Parkinson's disease: Blowing in the wind or not.Purinergic signalling · 2026Review
- The brain and heart-axis in neurodegeneration and cardiovascular disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- The ketogenic diet in Parkinson's disease: a potential therapeutic strategy.Pharmacological reports : PR · 2025Review
- Movement disorders: a brief overview from an evolutionary perspective.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Update on the Present and Future Pharmacologic Treatment of Parkinson's Disease.Neurology and therapy · 2025Review
- Levodopa treatment: impacts and mechanisms throughout Parkinson's disease progression.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Revolutionizing our understanding of Parkinson's disease: Dr. Heinz Reichmann's pioneering research and future research direction.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Clinicians' viewpoints on current paradigms of care and research in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Therapy with botulinum neurotoxin for Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Postencephalitic Parkinsonism: Unique Pathological and Clinical Features-Preliminary Data.Cells · 2024Article
- Exploring brain asymmetry in early-stage Parkinson's disease through functional and structural MRI.CNS neuroscience & therapeutics · 2024Article
- The vicious circle between homocysteine, methyl group-donating vitamins and chronic levodopa intake in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Toxic interactions between dopamine, α-synuclein, monoamine oxidase, and genes in mitochondria of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 14 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) comprises a spectrum of disorders with differing subtypes, the vast majority of which share Lewy bodies (LB) as a characteristic pathological hallmark. The process(es) underlying LB generation and its causal trigger molecules are not yet fully understood. α-Synuclein (α-syn) is a major component of LB and SNCA gene missense mutations or duplications/triplications are causal for rare hereditary forms of PD. As typical sporadic PD is associated with LB pathology, a factor of major importance is the study of the α-syn protein and its pathology. α-Syn pathology is, however, also evident in multiple system atrophy (MSA) and Lewy body disease (LBD), making it non-specific for PD. In addition, there is an overlap of these α-synucleinopathies with other protein-misfolding diseases. It has been proven that α-syn, phosphorylated tau protein (pτ), amyloid beta (Aβ) and other proteins show synergistic effects in the underlying pathogenic mechanisms. Multiple cell death mechanisms can induce pathological protein-cascades, but this can also be a reverse process. This holds true for the early phases of the disease process and especially for the progression of PD. In conclusion, while rare SNCA gene mutations are causal for a minority of familial PD patients, in sporadic PD (where common SNCA polymorphisms are the most consistent genetic risk factor across populations worldwide, accounting for 95% of PD patients) α-syn pathology is an important feature. Conversely, with regard to the etiopathogenesis of α-synucleinopathies PD, MSA and LBD, α-syn is rather a bystander contributing to multiple neurodegenerative processes, which overlap in their composition and individual strength. Therapeutic developments aiming to impact on α-syn pathology should take this fact into consideration.
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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.