Alpha-Synuclein in Neurological Diseases
A special issue of Neurology International (ISSN 2035-8377).
Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 299
Special Issue Editor
Interests: Parkinson’s disease; alpha-synuclein; autophagy-lysosome pathway; mitochondrial dysfunction; neuroinflammation
Special Issue Information
Dear Colleagues,
Alpha-synuclein (α-synuclein) is related to the pathogenesis of several neurodegenerative diseases, including Parkinson’s disease, dementia with Lewy bodies, multiple system atrophy, and other synucleinopathies. The normal function of α-synuclein is associated with the regulation of neurotransmitter vesicle trafficking, thereby maintaining neuronal presynaptic activity. Despite the deconformation of α-synuclein, synucleinopathies exhibit a slight relationship with the loss of function of α-synuclein. However, many studies have revealed that the aggregation of misfolded α-synuclein is mediated by the failure of the quality control system in cells, including proteasome degradation and the autophagy–lysosome pathway. In addition, the conformational modification of α-synuclein via intrinsic or extrinsic conditions, such as metal ion dyshomeostasis, reactive oxygen species, and lipid peroxidation, is also linked to the aggregation of α-synuclein. While the spatiotemporal dynamic of α-synuclein’s assembly to oligomeric, pre-fibrillar, and fibrillar formation is not yet fully elucidated, several studies have reported that the pre-fibrillar or oligomeric formation of α-synuclein is a culprit of mitochondrial dysfunction, failure of lysosomal activity, and toxicity in neuronal cells. In addition, the secretion of α-synuclein aggregates acts as cell-to-cell transmission, accelerates the aggregation of α-synuclein in the next neuron, and promotes neuroinflammatory responses via reactive astrocytes and microglia cells. Altogether, a comprehensive understanding of α-synuclein mechanisms and their interactions in intra- and extracellular space is important for the validation of therapeutic targets in disease initiation and progression. Hence, I look forward to receiving your contributions to this Special Issue, which aims to elucidate the pathological feature of α-synuclein by integrating the current knowledge and exploring the most recent advances within the field.
Prof. Dr. Dong Hwan Ho
Guest Editor
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Keywords
- alpha-synuclein
- Parkinson’s disease
- dementia with Lewy bodies
- multiple system atrophy
- protein misfolding
- protein quality control system
- autophagy–lysosome pathway
- mitochondrial dysfunction
- neuroinflammation
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