Proteomic Profiling of Exosomal Proteins for Blood-based Biomarkers in Parkinson's Disease

•CLU, C1R, and APOA1 in exosomes were decreased in PD at HY stages II and III.•Expression levels of APOA1 in exosomes reduced in correlation with severity of PD.•FGG in plasma was also decreased in PD patients at HY stages II and III. Parkinson’s disease (PD) is the second most common progressive ne...

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Published in:Neuroscience 2018-11, Vol.392, p.121-128
Main Authors: Kitamura, Yuki, Kojima, Midori, Kurosawa, Toshihito, Sasaki, Ryogen, Ichihara, Sahoko, Hiraku, Yusuke, Tomimoto, Hidekazu, Murata, Mariko, Oikawa, Shinji
Format: Article
Language:English
Subjects:
biomarkers
exosomes
Parkinson's disease
proteomics
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Summary:•CLU, C1R, and APOA1 in exosomes were decreased in PD at HY stages II and III.•Expression levels of APOA1 in exosomes reduced in correlation with severity of PD.•FGG in plasma was also decreased in PD patients at HY stages II and III. Parkinson’s disease (PD) is the second most common progressive neurodegenerative disorder and is characterized by loss of dopaminergic neurons. Biomarkers for tracking disease progression are useful indicators of the pathological conditions or the effects of therapeutic interventions on disease progression, but there are currently no known biomarkers in the blood that correlate with the progression of PD. Several studies have suggested that exosomes reflect intracellular changes that occur in response to pathological conditions and are an effective source of biomarkers for disease progression. To identify candidate biomarkers of disease progression in PD, we isolated exosomes from plasma of PD patients at Hoehn and Yahr (HY) stages II and III and performed protein profiling of the exosomes using two-dimensional differential gel electrophoresis (2D-DIGE). The expression levels of three proteins (clusterin, complement C1r subcomponent, and apolipoprotein A1) in PD patients at HY stages II and III were significantly decreased compared to healthy subjects (p 
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2018.09.017