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SHR Neuro Cancer Cardio Lipid Metab Microb

Wang, T; Hay, JC.
Alpha-synuclein Toxicity in the Early Secretory Pathway: How It Drives Neurodegeneration in Parkinsons Disease.
Front Neurosci. 2015; 9(3):433-433 Doi: 10.3389/fnins.2015.00433 [OPEN ACCESS]
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Leading authors Med Uni Graz
Hay Jesse
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Abstract:
Alpha-synuclein is a predominant player in the pathogenesis of Parkinson's Disease. However, despite extensive study for two decades, its physiological and pathological mechanisms remain poorly understood. Alpha-synuclein forms a perplexing web of interactions with lipids, trafficking machinery, and other regulatory factors. One emerging consensus is that synaptic vesicles are likely the functional site for alpha-synuclein, where it appears to facilitate vesicle docking and fusion. On the other hand, the dysfunctions of alpha-synuclein are more dispersed and numerous; when mutated or over-expressed, alpha-synuclein affects several membrane trafficking and stress pathways, including exocytosis, ER-to-Golgi transport, ER stress, Golgi homeostasis, endocytosis, autophagy, oxidative stress, and others. Here we examine recent developments in alpha-synuclein's toxicity in the early secretory pathway placed in the context of emerging themes from other affected pathways to help illuminate its underlying pathogenic mechanisms in neurodegeneration.

Find related publications in this database (Keywords)
alpha-synuclein
vesicle trafficking
golgi
ER stress response
neurodegenerative diseases
Parkinson disease
LRRK2
ER to golgi transport
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