ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Unbiased Proteomics of Early Lewy Body Formation Model Implicates Active Microtubule Affinity-Regulating Kinases (MARKs) in Synucleinopathies.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 41 citations in OpenAlex.
- The pesticide chlorpyrifos increases the risk of Parkinson's disease.Molecular neurodegeneration · 2025Article
- Differential role of C-terminal truncations on alpha-synuclein pathology and Lewy body formation.NPJ Parkinson's disease · 2025Article
- Pathological α-synuclein elicits granulovacuolar degeneration independent of tau.Translational neurodegeneration · 2025Article
- Broad proteomics analysis of seeding-induced aggregation of α-synuclein in M83 neurons reveals remodeling of proteostasis mechanisms that might contribute to Parkinson's disease pathogenesis.Molecular brain · 2024Article
- Disease Mechanisms of Multiple System Atrophy: What a Parallel Between the Form of Pasta and the Alpha-Synuclein Assemblies Involved in MSA and PD Tells Us.Cerebellum (London, England) · 2024Review
- Methods to Discover and Validate Biofluid-Based Biomarkers in Neurodegenerative Dementias.Molecular & cellular proteomics : MCP · 2023Article
- The roles of connectivity and neuronal phenotype in determining the pattern of α-synuclein pathology in Parkinson's disease.Neurobiology of disease · 2022Review
- A NAC domain mutation (E83Q) unlocks the pathogenicity of human alpha-synuclein and recapitulates its pathological diversity.Science advances · 2022Article
- Selectivity of Lewy body protein interactions along the aggregation pathway of α-synuclein.Communications biology · 2021Article
- Cerebrospinal Fluid Proteome Changes in Older Non-Cardiac Surgical Patients with Postoperative Cognitive Dysfunction.Journal of Alzheimer's disease : JAD · 2021Observational
- Microtubule affinity-regulating kinase 4 with an Alzheimer's disease-related mutation promotes tau accumulation and exacerbates neurodegeneration.The Journal of biological chemistry · 2020Article
- Glucocerebrosidase Activity Modulates Neuronal Susceptibility to Pathological α-Synuclein Insult.Neuron · 2020Article
- The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Characterization of novel conformation-selective α-synuclein antibodies as potential immunotherapeutic agents for Parkinson's disease.Neurobiology of disease · 2020Article
- Proteomics; applications in familial Parkinson's disease.Journal of neurochemistry · 2019Review
- α-Synuclein pathology in Parkinson's disease and related α-synucleinopathies.Neuroscience letters · 2019Review
- Composition of the Intranuclear Inclusions of Fragile X-associated Tremor/Ataxia Syndrome.Acta neuropathologica communications · 2019Article
- PARK14 (D331Y) PLA2G6 Causes Early-Onset Degeneration of Substantia Nigra Dopaminergic Neurons by Inducing Mitochondrial Dysfunction, ER Stress, Mitophagy Impairment and Transcriptional Dysregulation in a Knockin Mouse Model.Molecular neurobiology · 2019Article
- Beyond the synucleinopathies: alpha synuclein as a driving force in neurodegenerative comorbidities.Translational neurodegeneration · 2019Review
- A Druggable Genome Screen Identifies Modifiers of α-Synuclein Levels via a Tiered Cross-Species Validation Approach.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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8 authors at 2 institutions in 1 country.
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Abstract
Parkinson's disease (PD) patients progressively accumulate intracytoplasmic inclusions formed by misfolded α-synuclein known as Lewy bodies (LBs). LBs also contain other proteins that may or may not be relevant in the disease process. To identify proteins involved early in LB formation, we performed proteomic analysis of insoluble proteins in a primary neuron culture model of α-synuclein pathology. We identified proteins previously found in authentic LBs in PD as well as several novel proteins, including the microtubule affinity-regulating kinase 1 (MARK1), one of the most enriched proteins in this model of LB formation. Activated MARK proteins (MARKs) accumulated in LB-like inclusions in this cell-based model as well as in a mouse model of LB disease and in LBs of postmortem synucleinopathy brains. Inhibition of MARKs dramatically exacerbated α-synuclein pathology. These findings implicate MARKs early in synucleinopathy pathogenesis and as potential therapeutic drug targets.
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