Please use this identifier to cite or link to this item:
|Title:||Rabs, SNAREs and α-synuclein - Membrane trafficking defects in synucleinopathies|
Parkinson's disease (PD)
|Citation:||Chua, C.E.L., Tang, B.L. (2011-06-24). Rabs, SNAREs and α-synuclein - Membrane trafficking defects in synucleinopathies. Brain Research Reviews 67 (1-2) : 268-281. ScholarBank@NUS Repository. https://doi.org/10.1016/j.brainresrev.2011.03.002|
|Abstract:||Neuronal dysfunctions and neurodegeneration are often associated with defects in membrane transport. Synucleinopathies are a diverse group of neurodegenerative disorders that share a common pathological feature - insoluble aggregates composed largely of the protein α-synuclein in certain populations of neurons and glia. The actual physiological function of the brain-enriched α-synuclein is still not particularly clear. What is obvious is that when the protein is present in pathologically high amounts, or in mutant forms with enhanced membrane association and oligomerization, it causes neuronal demise with manifestations of impaired neuronal traffic, heightened oxidative stress, mitochondrial degeneration and defects in lipid metabolism α-synuclein's direct association with the activities of key components of the eukaryotic membrane traffic machinery, namely Rabs and the soluble N-ethylmaleimide sensitive factor (NSF) attachment protein receptors (SNAREs), has highlighted a key role for membrane transport defects in α-synuclein-mediated pathology. Here, we summarize and discuss recent findings in this regard, and their implications in the molecular aspects of synucleinopathy. © 2011 Elsevier B.V.|
|Source Title:||Brain Research Reviews|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Jun 19, 2018
WEB OF SCIENCETM
checked on Jun 11, 2018
checked on May 25, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.