ReviewCells2022
Alpha-Synuclein Aggregation Pathway in Parkinson's Disease: Current Status and Novel Therapeutic Approaches.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 4 of them syntheses that pooled it.
What it found
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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.
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
89 citing papers in PubMed, 4 syntheses or guidelines pooled it, 166 citations in OpenAlex.
- Actual Data on Essential Trace Elements in Parkinson's Disease.Nutrients · 2025Pooled it
- Implications of Butyrate Signaling Pathways on the Motor Symptomatology of Parkinson's Disease and Neuroprotective Effects-Therapeutic Approaches: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Pooled it
- The Role of Hydrogen Sulfide (HInternational journal of molecular sciences · 2023Pooled it
- Hyphenated Mass Spectrometry-Based Strategies for Characterizing Oligomers of α‑Synuclein in Parkinson's Disease.ACS central science · 2026Article
- Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.Neuromolecular medicine · 2026Review
- Cross-link Between CircRNAs and Neuroinflammation in Parkinson's Disease.Molecular neurobiology · 2026Review
- Nicotine in Neurodegenerative and Neuropsychiatric Disorders: Mechanisms and Clinical Evidence.Neurochemical research · 2026Review
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson's disease.Metabolic brain disease · 2026Review
- α-Synuclein as a molecular link between Parkinson's disease and chronic kidney disease: insights into the kidney-brain axis.Metabolic brain disease · 2026Review
- Microglia-derived extracellular vesicles attenuate acute a-synuclein induced astrocyte inflammation.bioRxiv : the preprint server for biology · 2026Article
- Copper Overload Affects α-Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model.Advanced biology · 2026Article
- Article
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
- Insight into the Neuroprotective Mechanisms of Resveratrol: Inhibition of Alpha-Synuclein Fibrillation and its Role in Mitigating Toxicity.Cell biochemistry and biophysics · 2026Article
- Drug screening for α-synuclein aggregation inhibitors via multimodal graph neural network.Briefings in bioinformatics · 2026Article
- Mitophagy-NLRP3 Inflammasome Crosstalk in Parkinson's Disease: Pathogenic Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Aesculus hippocastanum Extract Exerts Neuroprotective Effects in an MPPJournal of cellular and molecular medicine · 2026Article
- Evaluation of Hemodynamic and Blood Oxygen Metabolism Alterations in Parkinson's Disease Using Quantitative MRI.Current neuropharmacology · 2026Article
29 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following Alzheimer's, Parkinson's disease (PD) is the second-most common neurodegenerative disorder, sharing an unclear pathophysiology, a multifactorial profile, and massive social costs worldwide. Despite this, no disease-modifying therapy is available. PD is tightly associated with α-synuclein (α-Syn) deposits, which become organised into insoluble, amyloid fibrils. As a typical intrinsically disordered protein, α-Syn adopts a monomeric, random coil conformation in an aqueous solution, while its interaction with lipid membranes drives the transition of the molecule part into an α-helical structure. The central unstructured region of α-Syn is involved in fibril formation by converting to well-defined, β-sheet rich secondary structures. Presently, most therapeutic strategies against PD are focused on designing small molecules, peptides, and peptidomimetics that can directly target α-Syn and its aggregation pathway. Other approaches include gene silencing, cell transplantation, stimulation of intracellular clearance with autophagy promoters, and degradation pathways based on immunotherapy of amyloid fibrils. In the present review, we sum marise the current advances related to α-Syn aggregation/neurotoxicity. These findings present a valuable arsenal for the further development of efficient, nontoxic, and non-invasive therapeutic protocols for disease-modifying therapy that tackles disease onset and progression in the future.
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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.