Abstract:
:Free radicals, including dopamine (DA)-oxidized metabolites, have long been implicated in pathogenesis of Parkinson's disease (PD). However, the relationships between such oxidative stresses and alpha-synuclein (alpha-S), a major constituent of Lewy bodies, remain unknown. In this study, we established neuronal cells that constitutively express alpha-S and tetracycline-regulated tyrosinase. While tyrosinase overexpression induced apoptosis, co-expression of wild type or A53T mutant human alpha-S with tyrosinase further exacerbated cell death. In this process, the formation of alpha-S oligomers and the reduction in mitochondrial membrane potential were demonstrated. This cellular model may reconstitute the pathological metabolism of alpha-S in the synucleinopathy and provide a useful tool to explore possible pathomechanisms of nigral degeneration in PD.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Hasegawa T,Matsuzaki-Kobayashi M,Takeda A,Sugeno N,Kikuchi A,Furukawa K,Perry G,Smith MA,Itoyama Ydoi
10.1016/j.febslet.2006.03.018keywords:
subject
Has Abstractpub_date
2006-04-03 00:00:00pages
2147-52issue
8eissn
0014-5793issn
1873-3468pii
S0014-5793(06)00319-Xjournal_volume
580pub_type
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