Turning Points in α-Synuclein Biology: From Function to Dysfunction
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".
Deadline for manuscript submissions: 31 August 2026 | Viewed by 52
Special Issue Editors
Interests: mitochondrial biology; protein-protein and protein-lipid interactions; neurodegeneration; membrane organelle dynamics
Interests: α-synuclein aggregation and toxicity; mitochondrial dysfunction in neurodegeneration; endocytosis; cellular mechanisms underlying Parkinson’s disease
Special Issue Information
Dear Colleagues,
α-Synuclein sits at the nexus of neuronal function and neurodegeneration. Its balance between physiological and pathological activity shapes the course of synucleinopathies, including Parkinson’s disease. α-Synuclein can shift from a soluble, functional protein to toxic forms. This transition is regulated by post-translational modifications, genetic variations, and the cellular environment. These changes alter its interactions with functional and pathological partners. Even small perturbations can trigger cascading dysfunction, disrupting synaptic vesicle trafficking, mitochondrial homeostasis, proteostasis, and autophagy, ultimately leading to cell death.
Recent advances in modeling α-Synuclein protein behaviors in various cellular and animal models are beginning to map this complex network, showing how subtle changes can drive widespread cellular dysfunction. We invite submissions that probe the molecular switches controlling α-Synuclein pathological conversion, map its dynamic interactome, and link these events to neurotoxic pathways. This Special Issue seeks contributions that advance α-Synuclein biology and inform strategies to intercept disease at its earliest stages.
Dr. Quan Zhong
Dr. Ishita Haider
Guest Editors
Manuscript Submission Information
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Keywords
- α-synuclein
- protein aggregation
- pathological conversion
- synucleinopathies
- Parkinson’s disease
- neurodegeneration
- neurotoxicity
- proteostasis
- mitochondrial dysfunction
- autophagy
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