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ACCEPTED MANUSCRIPT dopaminergic neurons. These neurons are characterized by a high oxidative burden resulting from dopamine metabolism and excitotoxicity, while their antioxidative repertoire is rather limited (rev. in [18, 82]). In this context it is interesting to note that regiospecific differences in biochemical and structural parameters of brain mitochondria have been documented. Another key player seems to be calcium. Adult dopaminergic neurons are uniquely dependent on voltage-dependent L-type Ca 2+ channels for autonomous pacemaking activity [314-317]. In keeping with a crucial role of mitochondria in regulating calcium homeostasis, a dysbalance in calcium buffering seems to be causally related to the selective degeneration of dopaminergic neurons (rev.in [318]). Collectively, the exceptional physiological features of dopaminergic neurons help to explain why mitochondrial fidelity and an effective cellular quality control and stress response management are paramount to the survival of these neurons, particularly in an aging individual. There is compelling evidence that at least some of the PD-associated genes interface with these pathways . It will now be a challenging endeavour to exploit these pathways as a rationale to halt or delay disease progression and to move basic research into clinical practice. ACCEPTED MANUSCRIPT 37
Acknowledgements ACCEPTED MANUSCRIPT The work of the authors is supported by the Deutsche Forschungsgemeinschaft (SFB 596), German Ministry for Education and Research (NGFN plus "Functional Genomics of Parkinson's Disease"), the Helmholtz Alliance “Mental Health in an Ageing Society”, the Center for Integrated Protein Science Munich, and the Hans and Ilse Breuer Foundation. We thank Mareike E. Fett for providing Figure 2. ACCEPTED MANUSCRIPT 38
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