ArticleJournal of proteome research2021
Complement and Coagulation Cascades are Potentially Involved in Dopaminergic Neurodegeneration in α-Synuclein-Based Mouse Models of Parkinson's Disease.
Article in Journal of proteome research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Neuronal titration of Snca via enhancer disruption mitigates disease onset in a Parkinson's disease mouse model.Brain : a journal of neurology · 2026Article
- Complement dysregulation during the early phases of synucleinopathy.Acta neuropathologica · 2026Article
- The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.EBioMedicine · 2026Article
- Targeting central immune signaling enhances the effects of methylphenidate in alleviating apathy-like behavior in 5xFAD mice.Scientific reports · 2026Article
- Chronic sleep restriction activates complement and coagulation cascades: a molecular link to accelerated brain aging.Npj biological timing and sleep · 2026Article
- Deciphering Ferroptosis-Related Astrocyte Subpopulations and Diagnostic Biomarkers in Parkinson's Disease through RNA Transcriptomics.Molecular neurobiology · 2025Article
- Noradrenergic Slow Vasomotion: The Hidden Fluid Pump Linking Sleep, Brain Clearance, and Dementia Pathogenesis.International journal of molecular sciences · 2025Review
- Attenuating α-synuclein pathology in mice with in situ engineered astrocytes.Translational neurodegeneration · 2025Article
- Unique nigral and cortical pathways implicated by epigenomic and transcriptional analyses in rotenone Parkinson's model.NPJ Parkinson's disease · 2025Article
- Phosphoproteome modifications and cortical circuit dysfunction are linked to the early-stage progression of alpha-synuclein aggregation.bioRxiv : the preprint server for biology · 2025Article
- Phytochemicals in Parkinson's Disease: a Pathway to Neuroprotection and Personalized Medicine.Cell biochemistry and biophysics · 2025Review
- Complement C4 exacerbates astrocyte-mediated neuroinflammation and promotes α-synuclein pathology in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Stage-dependent proteomic alterations in aqueous humor of diabetic retinopathy patients based on data-independent acquisition and parallel reaction monitoring.Journal of translational medicine · 2025Article
- Chronic sleep curtailment expediates brain aging by activating the complement and coagulation cascades in mice.bioRxiv : the preprint server for biology · 2025Article
- Exploring Brain Imaging and Genetic Risk Factors in Different Progression States of Alzheimer's Disease Through OSnetNMF-Based Methods.Journal of molecular neuroscience : MN · 2025Article
- Glycine-to-aspartic acid mutation at codon 51 inBrain communications · 2025Article
- (Re)building the nervous system: A review of neuron-glia interactions from development to disease.Journal of neurochemistry · 2025Review
- A nomogram based on coagulation markers for predicting meige syndrome risk.Frontiers in aging neuroscience · 2025Article
- Non-canonical Roles of Complement in the CNS: From Synaptic Organizer to Presynaptic Modulator of Glutamate Transmission.Current neuropharmacology · 2025Review
- Dysregulated Coagulation in Parkinson's Disease.Cells · 2024Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 3 countries.
Funding
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disorder that results in motor dysfunction and, eventually, cognitive impairment. α-Synuclein protein is known as a central protein to the pathophysiology of PD, but the underlying pathological mechanism still remains to be elucidated. In an effort to understand how α-synuclein underlies the pathology of PD, various PD mouse models with α-synuclein overexpression have been developed. However, systemic analysis of the brain proteome of those mouse models is lacking. In this study, we established two mouse models of PD by injecting α-synuclein preformed fibrils (PFF) or by inducing overexpression of human A53T α-synuclein to investigate common pathways in the two different types of the PD mouse models. For more accurate quantification of mouse brain proteome, the proteins were quantified using the method of stable isotope labeling with amino acids in mammals . We identified a total of 8355 proteins from the two mouse models; ∼6800 and ∼7200 proteins from α-synuclein PFF-injected mice and human A53T α-synuclein transgenic mice, respectively. Through pathway analysis of the differentially expressed proteins common to both PD mouse models, it was discovered that the complement and coagulation cascade pathways were enriched in the PD mice compared to control animals. Notably, a validation study demonstrated that complement component 3 (C3)-positive astrocytes were increased in the ventral midbrain of the intrastriatal α-synuclein PFF-injected mice and C3 secreted from astrocytes could induce the degeneration of dopaminergic neurons. This is the first study that highlights the significance of the complement and coagulation pathways in the pathogenesis of PD through proteome analyses with two sophisticated mouse models of PD.
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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.