ArticleScientific reports2015
Cofilin 1 activation prevents the defects in axon elongation and guidance induced by extracellular alpha-synuclein.
Article in Scientific reports, 2015. 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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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
22 citing papers in PubMed, 41 citations in OpenAlex.
- Label-free proteomic profiling identifies ECM-related alterations across regeneration states in human peripheral axonal neuropathies.Journal of physiology and biochemistry · 2026Article
- Exploring the Neuroprotective Role of Selenium: Implications and Perspectives for Central Nervous System Disorders.Exploration (Beijing, China) · 2025Review
- Evaluating the Role of Lin-11, Isl-1, and Mec-3 Kinases in Dopaminergic Neurodegeneration in a Subacute 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Parkinson's Disease.ACS pharmacology & translational science · 2024Article
- Role of Rho-associated kinases and their inhibitor fasudil in neurodegenerative diseases.Frontiers in neuroscience · 2024Review
- β-Actin: An Emerging Biomarker in Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- Promising biomarkers and therapeutic targets for the management of Parkinson's disease: recent advancements and contemporary research.Metabolic brain disease · 2023Review
- Multiomic Analysis of Neurons with Divergent Projection Patterns Identifies Novel Regulators of Axon Pathfinding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Changes in nanomechanical properties of single neuroblastoma cells as a model for oxygen and glucose deprivation (OGD).Scientific reports · 2022Article
- Emerging Therapeutic Strategies for Parkinson's Disease and Future Prospects: A 2021 Update.Biomedicines · 2022Review
- Examining the Toxicity of α-Synuclein in Neurodegenerative Disorders.Life (Basel, Switzerland) · 2021Review
- Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021Review
- Linking Alpha-Synuclein to the Actin Cytoskeleton: Consequences to Neuronal Function.Frontiers in cell and developmental biology · 2020Review
- Semaphorin-3A Promotes Degradation of Fragile X Mental Retardation Protein in Growth ConesFrontiers in neural circuits · 2020Article
- A Subtle Network Mediating Axon Guidance: Intrinsic Dynamic Structure of Growth Cone, Attractive and Repulsive Molecular Cues, and the Intermediate Role of Signaling Pathways.Neural plasticity · 2019Review
- Article
- IRES-mediated translation of cofilin regulates axonal growth cone extension and turning.The EMBO journal · 2018Article
- Regulation of RhoA activity by the cellular prion protein.Cell death & disease · 2017Article
- α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies.Nature medicine · 2017Review
- Actin Waves Do Not Boost Neurite Outgrowth in the Early Stages of Neuron Maturation.Frontiers in cellular neuroscience · 2017Article
- Geometrical Determinants of Neuronal Actin Waves.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Impaired adult neurogenesis and axon traumatic injury participate in the severity of neurodegenerative diseases. Alpha-synuclein, a cytosolic protein involved in Parkinson's disease, may be released from neurons, suggesting a role for excess secreted alpha-synuclein in the onset and spread of the pathology. Here we provide evidence that long term exposure of young neurons to extracellular alpha-synuclein hampers axon elongation and growth cone turning. We show that actin turnover and the rate of movement of actin waves along the axon are altered, due to alpha-synuclein-induced inactivation of cofilin. Upon laser disruption of microfilaments, healing of axons is favored by the increased phosphorylation of cofilin, however, at later time points; the defect in neurite extension prevails, being lost the regulation of cofilin activity. Importantly, overexpression of the active form of cofilin in neurons exposed to alpha-synuclein is able to restore the movement of actin waves, physiological axon elongation and growth cone turning. Our study reveals the molecular basis of alpha-synuclein-driven deficits in growth and migration of newborn neurons, and in elongation and regeneration of adult neurons.
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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.