ReviewInternational journal of molecular sciences2024
The Role of α-Synuclein in Etiology of Neurodegenerative Diseases.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Postbiotics as a therapeutic frontier in Parkinson's disease: Insights into molecular pathways and neuroprotective effects.Metabolic brain disease · 2026Review
- Dexpanthenol Attenuates High Fructose Corn Syrup-Induced Brain Injury by Modulating Oxidative Stress, Neuroinflammation, Apoptotic Signaling and Amyloidogenic Gene Expression.Molecular neurobiology · 2026Article
- Proteo-metabolomic integration identifies stage-specific candidate biomarkers for Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Loss-of-Function (G603R) Lrp10 Fails to Downregulate mRNA of Pathologic α-Synuclein and Causes Neurodegeneration of Substantia Nigra Dopaminergic Cells in Parkinson's Disease Knockin Mice.Neurochemical research · 2026Article
- von Willebrand Factor fibers formed at pathological high shear provide a scaffold for α-synuclein binding and aggregation.Scientific reports · 2026Article
- Multi-parameter fluorescence lifetime imaging for high-noise neuroscience applications.Biomedical optics express · 2026Article
- The ketogenic diet in Parkinson's disease: mechanisms, evidence, and clinical practice.Frontiers in nutrition · 2026Review
- The role of exosomes as oligonucleotide delivery system for managing α-synuclein in Parkinson's disease: A systematic review ofMolecular therapy. Nucleic acids · 2025Article
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Nanomaterial-based approaches to neurotoxin neutralization in neurodegenerative diseases.Nanomedicine (London, England) · 2025Review
- Unravelling the Proteinopathic Engagement of α-Synuclein, Tau, and Amyloid Beta in Parkinson's Disease: Mitochondrial Collapse as a Pivotal Driver of Neurodegeneration.Neurochemical research · 2025Review
- Protein Misfolding in the Pathogenesis and Diagnosis of Neurodegenerative Diseases (Review).Sovremennye tekhnologii v meditsine · 2025Review
- Stem-cell-derived extracellular vesicles in neurodegeneration and neuroaging: therapeutic potential and challenges.Extracellular vesicles and circulating nucleic acids · 2025Review
- Mitochondrial stress disassembles nuclear architecture through proteolytic activation of PKCδ and Lamin B1 phosphorylation in neuronal cells: implications for pathogenesis of age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2025Article
- Precision Medicine in Neurodegenerative Diseases: Genomic Approaches to Target Amyloid-β, Tau, and Alpha-Synuclein Pathways.Current genomics · 2025Review
- Protective Effects of Ambroxol on Aβ and α-Synuclein-Induced Neurotoxicity Through Glucocerebrosidase Activation in HT-22 Hippocampal Neuronal Cells.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
A presynaptic protein called α-synuclein plays a crucial role in synaptic function and neurotransmitter release. However, its misfolding and aggregation have been implicated in a variety of neurodegenerative diseases, particularly Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Emerging evidence suggests that α-synuclein interacts with various cellular pathways, including mitochondrial dysfunction, oxidative stress, and neuroinflammation, which contributes to neuronal cell death. Moreover, α-synuclein has been involved in the propagation of neurodegenerative processes through prion-like mechanisms, where misfolded proteins induce similar conformational changes in neighboring neurons. Understanding the multifaced roles of α-synuclein in neurodegeneration not only aids in acquiring more knowledge about the pathophysiology of these diseases but also highlights potential biomarkers and therapeutic targets for intervention in alpha-synucleinopathies. In this review, we provide a summary of the mechanisms by which α-synuclein contributes to neurodegenerative processes, focusing on its misfolding, oligomerization, and the formation of insoluble fibrils that form characteristic Lewy bodies. Furthermore, we compare the potential value of α-synuclein species in diagnosing and differentiating selected neurodegenerative diseases.
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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.