الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
One of the most severe neurodegenerative disorders is Parkinson Disease.The pathogenesis of this illness involves tremor, impaired movement, and metabolic deficit. The signal pathways involved in metabolic deficit are still unknown, Here in this study I focus on metabolic defects Rotenone-induced Drosophila model of Parkinson Disease (PD). First of all, I confirmed the involvements of 13 genes with an important role in metabolism in Drosophila model of PD. This was achieved by determining the expression level of certain genes using RT PCR in rotenone-supplemented flies as compared to control. This study focus on the role played by these genes in controlling metabolism of PD model using RNAi knocking down of the corresponding genes. Results showed that levels of expression had shifted, either up or down, proving that those genes are implicated in the PD model of Drosophila. Next, metabolic parameters, rate of food consumption and defecation in flies that’s knocking down in the corresponding genes were evaluated. Results revealed that some of tested genes affected the external morphology. Regarding to feeding rate of some genes was significantly decreased in CG17544, CG16848, CG8417, CG10581, CG9391andCG5103 as compared to control . This suggests that these genes may act to limit food intake exactly as occurred during PD in humans. In comparison to control, there was a considerable decrease in the number of faecal pellets produced by the CG 8417, CG12913, and CG16848 -deficient flies. Such results suggest that these genes are linked to defecation rate disorder in Drosophila model of PD. Then the total protein, lipid, and carbohydrate contents in the Drosophila model of Parkinson’s disease were examined to provide insight into whether the tested genes had an impact on metabolism. Results indicated that certain genes were altered by metabolic factors as compared to control. This knowledge may be useful for pharmacotherapeutic strategies that enhance metabolism to enhance PD patients’ quality of life.