Brain proteasomal function in sporadic Parkinson's disease and related disorders
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Updated: Sep 30, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
Published on: October 3, 2012
Yoshiaki Furukawa1, Sophie Vigouroux, Henry Wong
1Movement Disorders Research Laboratory, Centre for Addiction and Mental Health-Clarke Division, 250 College Street, Toronto, Ontario, Canada M5T 1R8. yoshiaki_furukawa@camh.net
Abstract:
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.
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