Changes in the solubility and phosphorylation of α-synuclein over the course of Parkinson’s disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-03-13

AUTHORS

Jinxia Zhou, Melissa Broe, Yue Huang, John P. Anderson, Wei-Ping Gai, Elizabeth A. Milward, Michelle Porritt, David Howells, Andrew J. Hughes, Xiaomin Wang, Glenda M. Halliday

ABSTRACT

Lewy bodies are made from insoluble, phosphorylated α-synuclein, but the earliest changes that precipitate such pathology still remain conjecture. In this study, we quantify and identify relationships between the levels of the main pathologic form of phosphorylated α-synuclein over the course of Parkinson’s disease in regions affected early through to end-stage disease. Brain tissue samples from 33 cases at different disease stages and 13 controls were collected through the Australian Network of Brain Banks. 500 mg of frozen putamen (affected preclinically) and frontal cortex (affected late) was homogenized, fractionated and α-synuclein levels evaluated using specific antibodies (syn-1, BD Transduction Laboratories; S129P phospho-α-synuclein, Elan Pharmaceuticals) and quantitative western blotting. Statistical analyses assessed the relationship between the different forms of α-synuclein, compared levels between groups, and determined any changes over the disease course. Soluble S129P was detected in controls with higher levels in putamen compared with frontal cortex. In contrast, insoluble α-synuclein occurred in Parkinson’s disease with a significant increase in soluble and lipid-associated S129P, and a decrease in soluble frontal α-synuclein over the disease course. Increasing soluble S129P in the putamen correlated with increasing S129P in other fractions and regions. These data show that soluble non-phosphorylated α-synuclein decreases over the course of Parkinson’s disease, becoming increasingly phosphorylated and insoluble. The finding that S129P α-synuclein normally occurs in vulnerable brain regions, and in Parkinson’s disease has the strongest relationships to the pathogenic forms of α-synuclein in other brain regions, suggests a propagating role for putamenal phospho-α-synuclein in disease pathogenesis. More... »

PAGES

695-704

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00401-011-0815-1

DOI

http://dx.doi.org/10.1007/s00401-011-0815-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048182540

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21400129


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66 form
67 fraction
68 frontal cortex
69 frozen putamen
70 group
71 high levels
72 increase
73 levels
74 lipid-associated S129P
75 main pathologic form
76 network
77 pathogenesis
78 pathogenic form
79 pathologic forms
80 pathology
81 phospho
82 phosphorylation
83 putamen
84 putamenal phospho
85 quantitative Western blotting
86 region
87 relationship
88 role
89 significant increase
90 solubility
91 specific antibodies
92 stage
93 statistical analysis
94 strong relationship
95 study
96 such pathology
97 synuclein
98 synuclein decreases
99 synuclein levels
100 tissue
101 vulnerable brain regions
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