identification of bilateral changes in tid1 expression in the 6-ohda rat model of parkinsons disease双边tid1表达变化的识别6-ohda帕金森病大鼠模型.pdfVIP

Identification of Bilateral Changes in TID1 Expression in the 6-OHDA Rat Model of Parkinson’s Disease 1. 2,3. 2 2 1 Juliane Proft , Jamshid Faraji , Jerrah C. Robbins , Fabiola C. R. Zucchi , Xiaoxi Zhao , Gerlinde A. 2. 1 . Metz , Janice E. A. Braun * 1 Hotchkiss Brain Institute, Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada, 2 Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Canada, 3 Neuroscience Research Centre, Golestan University of Medical Sciences, Gorgan, Islamic Republic of Iran Abstract Parkinson’s disease (PD) is a common neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra and the aggregation of a-synuclein into Lewy bodies. Existing therapies address motor dysfunction but do not halt progression of the disease. A still unresolved question is the biochemical pathway that modulates the outcome of protein misfolding and aggregation processes in PD. The molecular chaperone network plays an important defensive role against cellular protein misfolding and has been identified as protective in experimental models of protein misfolding diseases like PD. Molecular mechanisms underlying chaperone-neuroprotection are actively under investigation. Current evidence implicates a number of molecular chaperones in PD including Hsp25, Hsp70 and Hsp90, however their precise involvement in the neurodegenerative cascade is unresolved. The J protein family (DnaJ or Hsp40 protein family) has long been known to be important in protein conformational processes. We assessed sensory and motor function of control and PD rats and then evaluated the br