Decreased alpha-synuclein in cerebrospinal fluid of aged individuals and subjects with Parkinson's disease. Export

@article{citeulike:4271365, abstract = {There is ample biochemical, pathological, and genetic evidence that the metabolism of alpha-synuclein (alpha-syn) plays a crucial role in the pathogenesis of Parkinson disease (PD). To examine whether quantification of alpha-syn in cerebrospinal fluid (CSF) is potentially informative in the diagnosis of PD, we developed a specific ELISA system and measured the concentration of alpha-syn in CSF from 33 patients with PD (diagnosed according to UK PD Society Brain Bank criteria) and 38 control subjects including 9 neurologically healthy individuals. We found that PD patients had significantly lower alpha-syn levels in their CSF than the control groups (p<0.0001) even after adjusting for gender and age. Age was independently associated with lower alpha-syn levels. Logistic regression analysis showed that reduction in CSF alpha-syn served as a significant predictor of PD beyond age and gender alone (area under ROC curve, c=0.882). Furthermore, we observed a close inverse correlation between alpha-syn levels in CSF and assigned Hoehn and Yahr score in this cohort of 71 living subjects (p<0.0001), even after adjusting for age. These findings identify in the quantification of alpha-syn from CSF a potential laboratory marker to aid the clinical diagnosis of PD.}, author = {Tokuda, T. and Salem, S. A. and Allsop, D. and Mizuno, T. and Nakagawa, M. and Qureshi, M. M. and Locascio, J. J. and Schlossmacher, M. G. and El-Agnaf, O. M.}, citeulike-article-id = {4271365}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.bbrc.2006.08.024}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16930553}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16930553}, day = {13}, doi = {10.1016/j.bbrc.2006.08.024}, issn = {0006-291X}, journal = {Biochemical and biophysical research communications}, keywords = {pd, synuclein}, month = {October}, number = {1}, pages = {162--166}, posted-at = {2009-04-04 01:42:08}, priority = {2}, title = {Decreased alpha-synuclein in cerebrospinal fluid of aged individuals and subjects with Parkinson's disease.}, url = {http://dx.doi.org/10.1016/j.bbrc.2006.08.024}, volume = {349}, year = {2006} }

TY - JOUR ID - citeulike:4271365 L3 - citeulike-article-id:4271365 N2 - There is ample biochemical, pathological, and genetic evidence that the metabolism of alpha-synuclein (alpha-syn) plays a crucial role in the pathogenesis of Parkinson disease (PD). To examine whether quantification of alpha-syn in cerebrospinal fluid (CSF) is potentially informative in the diagnosis of PD, we developed a specific ELISA system and measured the concentration of alpha-syn in CSF from 33 patients with PD (diagnosed according to UK PD Society Brain Bank criteria) and 38 control subjects including 9 neurologically healthy individuals. We found that PD patients had significantly lower alpha-syn levels in their CSF than the control groups (p<0.0001) even after adjusting for gender and age. Age was independently associated with lower alpha-syn levels. Logistic regression analysis showed that reduction in CSF alpha-syn served as a significant predictor of PD beyond age and gender alone (area under ROC curve, c=0.882). Furthermore, we observed a close inverse correlation between alpha-syn levels in CSF and assigned Hoehn and Yahr score in this cohort of 71 living subjects (p<0.0001), even after adjusting for age. These findings identify in the quantification of alpha-syn from CSF a potential laboratory marker to aid the clinical diagnosis of PD. IS - 1 JF - Biochemical and biophysical research communications SN - 0006-291X EP - 166 TI - Decreased alpha-synuclein in cerebrospinal fluid of aged individuals and subjects with Parkinson's disease. VL - 349 SP - 162 KW - pd KW - synuclein AU - Tokuda, T AU - Salem, SA AU - Allsop, D AU - Mizuno, T AU - Nakagawa, M AU - Qureshi, MM AU - Locascio, JJ AU - Schlossmacher, MG AU - El-Agnaf, OM PY - 2006/10/13/ UR - http://dx.doi.org/10.1016/j.bbrc.2006.08.024 ER -