Brain proteasomal function in sporadic Parkinson's disease and related disorders
Article first published online: 3 MAY 2002
Copyright © 2002 Wiley-Liss, Inc.
Annals of Neurology
Volume 51, Issue 6, pages 779–782, June 2002
How to Cite
Furukawa, Y., Vigouroux, S., Wong, H., Guttman, M., Rajput, A. H., Ang, L., Briand, M., Kish, S. J. and Briand, Y. (2002), Brain proteasomal function in sporadic Parkinson's disease and related disorders. Ann Neurol., 51: 779–782. doi: 10.1002/ana.10207
- Issue published online: 21 MAY 2002
- Article first published online: 3 MAY 2002
- Manuscript Accepted: 9 FEB 2002
- Manuscript Revised: 6 FEB 2002
- Manuscript Received: 27 NOV 2001
- William S. Storey and Al Silverberg PSP Funds
- Friedman MSA Fund
- Centre for Addiction and Mental Health Foundation
Because genetic defects relating to the ubiquitin–proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.