**1. Introduction**

292 Etiology and Pathophysiology of Parkinson's Disease

Valente, E.M.; Abou-Sleiman, P.M.; Caputo, V.; Muqit, M.M.; Harvey, K.; Gispert, S.; Ali, Z.;

Vannucci, S.J.; Maher, F.& Simpson, I.A. (1997). Glucose transporter proteins in brain:

Virmani, M.A.; Biselli, R.; Spadoni, A.; Rossi, S.; Corsico, N.; Calvani, M.; Fattorossi, A.; De

Wallace, D.C.; Shoffner, J.M.; Watts, R.L.; Juncos, J.L.& Torroni, A. (1992). Mitochondrial

Winklhofer, K.F. & Haass, C. (2010). Mitochondrial dysfunction in Parkinson's disease.

Woods, J.W.; Tanen, M.; Figueroa, D.J.; Biswas, C.; Zycband, E.; Moller, D.E.; Austin, C.P.&

Yang, S.Y.; He, X.Y.& Schulz, H. (2005). 3-Hydroxyacyl-CoA dehydrogenase and short chain

Yoon, J.C.; Puigserver, P.; Chen, G.; Donovan, J.; Wu, Z.; Rhee, J.; Adelmant, G.; Stafford, J.;

Yoshino, H.; Nakagawa-Hattori, Y.; Kondo, T.& Mizuno, Y. (1992). Mitochondrial complex I

*Neural Transmission.Parkinson's disease and Dementia Section,* Vol.4, pp. 27-34 Zheng, B. et al. (2010). PGC-1alpha, a potential therapeutic target for early intervention in

Zimprich, A. et al.(2004). Mutations in LRRK2 cause autosomal-dominant parkinsonism

Zschocke, J.; Ruiter, J.P.; Brand, J.; Lindner, M.; Hoffmann, G.F.; Wanders, R.J.& Mayatepek,

Parkinson's disease. *Science Translational Medicine,* Vol.2, pp. 52ra73

with pleomorphic pathology. *Neuron,* Vol.44, pp. 601-607

delivery of glucose to neurons and glia. *Glia,* Vol.21, pp. 2-21

inhibitors. *Pharmacological Research,* Vol.32, pp. 383-389

*Biochimica et Biophysica Acta,* Vol.1802, pp. 29-44

1158-1160

Vol.32, pp. 113-114

PGC-1. *Cell,* Vol.98, pp. 115-124

Vol.272, pp. 4874-4883

Vol.413, pp. 131-138

Del Turco, D.; Bentivoglio, A.R.; Healy, D.G.; Albanese, A.; Nussbaum, R.; Gonzalez-Maldonado, R.; Deller, T.; Salvi, S.; Cortelli, P.; Gilks, W.P.; Latchman, D.S.; Harvey, R.J.; Dallapiccola, B.; Auburger, G.& Wood, N.W. (2004). Hereditary early-onset Parkinson's disease caused by mutations in PINK1. *Science,* Vol.304, pp.

Simone, C.& Arrigoni-Martelli, E. (1995). Protective actions of L-carnitine and acetyl-L-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or

oxidative phosphorylation defects in Parkinson's disease. *Annals of Neurology,*

Berger, J.P. (2003). Localization of PPARdelta in murine central nervous system: expression in oligodendrocytes and neurons. *Brain Research,* Vol.975, pp. 10-21 Wu, Z.; Puigserver, P.; Andersson, U.; Zhang, C.; Adelmant, G.; Mootha, V.; Troy, A.; Cinti,

S.; Lowell, B.; Scarpulla, R.C.& Spiegelman, B.M. (1999). Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator

3-hydroxyacyl-CoA dehydrogenase in human health and disease. *FEBS Journal,*

Kahn, C.R.; Granner, D.K.; Newgard, C.B.& Spiegelman, B.M. (2001). Control of hepatic gluconeogenesis through the transcriptional coactivator PGC-1. *Nature,*

and II activities of lymphocytes and platelets in Parkinson's disease. *Journal of* 

E. (2000). Progressive infantile neurodegeneration caused by 2-methyl-3 hydroxybutyryl-CoA dehydrogenase deficiency: a novel inborn error of branchedchain fatty acid and isoleucine metabolism. *Pediatric Research,* Vol.48, pp. 852-855

The information that stems from the primary structure of DNA lies within the basis of every sign formation, although the regulation of any process occurs in different levels of cellular processes including transcription. In this context analysis of gene transcription is of great importance to improve our understanding of the pathogenesis of diverse disorders, and Parkinson's disease (PD) is not an exception. However, each disease has its own unique etiopathogenesis within organs and tissues, which is caused by disease-specific processes in cells, as well as at the genetic level. Knowledge of the etiology and pathogenesis of diseases at a cellular level opens wide prospects for diagnosis and treatment, even for complex and incurable disorders such as PD. Therefore, it is necessary to study the pathogenesis of specific disease at the cellular and genetic levels. Accordingly, the expression profiles of large numbers of genes are being studied in different neurodegenerative disorders, including PD. Although the mechanisms that initiate neuronal pathology in sporadic PD remain largely obscure, in this chapter we have tried to summarize all current knowledge in the field of the PD transcriptomics.
