A large body of evidence implicates a central role for mitochondrial dysfunction in the pathogenesis of Parkinson's disease (PD), though the precise causes of mitochondrial dysfunction in PD remain to be determined. Mitochondrial complex I activity is impaired in the substantia nigra at early stages in PD. This complex I dysfunction appears not to be simply a consequence of neurodegeneration as toxins that inhibit mitochondrial complex I can reproduce many of the key pathological features of PD in animal models. Several genetic causes of PD have been linked directly or indirectly to mitochondrial function, and thus a convergence of data highlight the role of mitochondrial dysfunction in PD.

We are particularly interested in reviews that critically evaluate the scientific literature in cellular and animal models of Parkinson's disease. Manuscripts that focus on data from human studies also are welcome. Papers focusing on oxidative stress will be considered if they address the role of mitochondria as the source or target of oxidative stress. We encourage both reviews as well as manuscripts that present original data. Main topics include, but are not limited to:

• Mitochondrial toxins
• Mitophagy
• Mitochondrial Fusion/Fission and Transport
• Mitochondria and calcium homeostasis
• Imaging (e.g., MRS)
• Oxidative stress
• Link between genetic causes of PD and mitochondrial dysfunction (alpha-synuclein, parkin, DJ-1, PINK1, etc.)
• Role of genetic variations in components of the respiratory enzyme chain in Parkinson's disease
• Inherited mtDNA mutations
• Somatic mtDNA mutations
• Mitochondria as targets for neuroprotection (uncouplers, PGC-1alpha, CoQ10, etc.)

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/pd/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: