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Oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase l1 associated with idiopathic.
| Content Provider | CiteSeerX |
|---|---|
| Abstract | are the two most common neurodegenerative diseases that occur either in relatively rare, familial forms or in common, sporadic forms. The genetic defects underly-ing several monogenic familial forms of AD and PD have recently been identified, however, the causes of other AD and PD cases, particularly sporadic cases, remain unclear. To gain insights into the pathogenic mecha-nisms involved in AD and PD, we used a proteomic ap-proach to identify proteins with altered expression lev-els and/or oxidative modifications in idiopathic AD and PD brains. Here, we report that the protein level of ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), a neuronal de-ubiquitinating enzyme whose mutation has been linked to an early-onset familial PD, is down-regu-lated in idiopathic PD as well as AD brains. By using a |
| File Format | |
| Access Restriction | Open |
| Subject Keyword | Oxidative Modification Ubiquitin Carboxyl-terminal Hydrolase L1 Associated Idiopathic Ad Protein Level Pd Brain Common Neurodegenerative Disease Sporadic Form Sporadic Case Pd Case Ad Brain Altered Expression Lev-els Familial Form Neuronal De-ubiquitinating Enzyme Pathogenic Mecha-nisms Proteomic Ap-proach Early-onset Familial Pd Ubiquitin Carboxyl-terminal Hydrolase L1 Idiopathic Pd |
| Content Type | Text |
