| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2014: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
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| Outline of Final Research Achievements |
In general, the pathology of Parkinson disease(PD) has been implicated in oxidative damage and mitochondrial dysfunction, which are probably induced by both genetic predisposition and environmental factors. Recent discovery of genes associated with the etiology of familial PD has emphasized the role of autophagy lysosomal system. PINK1, Parkin and ATP13A2 have been identified as the causal genes responsible for hereditary early onset PD. Mechanistic insights into mitochondrial quality control mediated by PINK1 and Parkin have been revealed. In the process of mitochondria degradation (mitophagy), PINK1 dependent phosphorylation of Parkin is essential for accelerating E3 ligase activity of Parkin. On the other hands, ATP13A2 localizes in lysosome and regulates enzyme activity including cathepsin D. Autophagy lysosomal dysfunction may be the common pathogenesis of early onset PD.
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