ReviewBrain communications2022
Linking α-synuclein-induced synaptopathy and neural network dysfunction in early Parkinson's disease.
Review in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 52 citations in OpenAlex.
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- Transcriptional dysregulation in the cerebellum triggered by oligodendroglial α-synucleinopathy: insights from a transgenic mouse into the early disease mechanisms of MSA.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Lipid Acyl Chain-Driven α-Synuclein Fibril Polymorphisms and Neuronal Pathologies.ACS chemical neuroscience · 2026Article
- New insights into synaptic vesicle dysfunction in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Article
- Characteristics and mechanisms of cognitive impairment in Parkinson disease.Nature reviews. Neurology · 2026Review
- Optogenetic-induced α-synuclein accumulation reveals early synaptic dysfunction in experimental models of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Pathway Analysis and Genetic Markers in Parkinson's Disease: Insights into Subtype-Specific Mechanisms.Molecular neurobiology · 2025Article
- Oligomeric alpha-synuclein causes early synaptic dysfunction of the corticostriatal pathway associated with non-motor symptoms.NPJ Parkinson's disease · 2025Article
- Key Connectomes and Synaptic-Compartment-Specific Risk Genes Drive Pathological α-Synuclein Spreading.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
- The Effect of Advancing Age and Intraocular Pressure Injury on Retinal Ganglion Cell Function and Synaptic Connectivity.Aging cell · 2025Article
- Multiplexed Dark FRET Biosensors: An accessible live-cell platform for target- and cell-specific monitoring of protein-protein interactions in 2D and 3D model systems.Research square · 2025Article
- Motor cortical neuronal hyperexcitability associated with α-synuclein aggregation.NPJ Parkinson's disease · 2025Article
- Prevalence, associated factors and impact of mild cognitive impairment in hospitalized older adults with Parkinson's disease: a cross-sectional study.Frontiers in aging neuroscience · 2025Article
- α-synuclein and tau: interactions, cross-seeding, and the redefinition of synucleinopathies as complex proteinopathies.Frontiers in neuroscience · 2025Review
- Spatiotemporal crosstalk among mitochondrial dynamics, NLRP3 inflammasome activation, and histone lactylation drivesFrontiers in cellular neuroscience · 2025Review
- BAG3's dual roles in Parkinson's disease and cardiomyopathy: benefit or liability?Acta neuropathologica · 2024Article
- Mitochondrial Dysfunction in Parkinson's Disease: A Contribution to Cognitive Impairment?International journal of molecular sciences · 2024Review
- Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation.Research square · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The prodromal phase of Parkinson's disease is characterized by aggregation of the misfolded pathogenic protein α-synuclein in select neural centres, co-occurring with non-motor symptoms including sensory and cognitive loss, and emotional disturbances. It is unclear whether neuronal loss is significant during the prodrome. Underlying these symptoms are synaptic impairments and aberrant neural network activity. However, the relationships between synaptic defects and network-level perturbations are not established. In experimental models, pathological α-synuclein not only impacts neurotransmission at the synaptic level, but also leads to changes in brain network-level oscillatory dynamics-both of which likely contribute to non-motor deficits observed in Parkinson's disease. Here we draw upon research from both human subjects and experimental models to propose a 'synapse to network prodrome cascade' wherein before overt cell death, pathological α-synuclein induces synaptic loss and contributes to aberrant network activity, which then gives rise to prodromal symptomology. As the disease progresses, abnormal patterns of neural activity ultimately lead to neuronal loss and clinical progression of disease. Finally, we outline goals and research needed to unravel the basis of functional impairments in Parkinson's disease and other α-synucleinopathies.
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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.