Mitochondria are intracellular organelles, which play a crucial role in energy metabolism. Most of cell energy is obtained through mitochondrial metabolic pathways, especially Krebs' cycle and electron transport chain which is the main site of reactive oxygen species production such as superoxide, hydrogen peroxide, and hydroxyl radicals. Brain is highly sensitive to oxidative stress due to its high oxygen consumption, iron and lipid contents, and low activity of antioxidant defenses. Thus, energy metabolism impairment and oxidative stress are important events that have been related to the pathogenesis of diseases affecting the central nervous system. Moreover, mitochondria are also key regulators of cell survival and death and play a central role in ageing. Further investigation in this subject will clarify several aspects in pathophysiology of neurodegenerative diseases.

We invite authors to submit original research and review articles that seek to refine the understanding of the role of mitochondrial dysfunction, energy metabolism impairment, and oxidative stress in pathophysiology of neurodegenerative diseases. Potential topics include, but are not limited to:

• Alzheimer's, Parkinson's, and Huntington's disease and mitochondrial dysfunction and oxidative stress
• Role of mitochondrial dysfunction/oxidative stress in pathophysiology of metabolic inherited disorders and psychiatric disorders
• Pharmacological interactions of drugs used to treat neurodegenerative disorders with tissue and mitochondrial structure, biochemistry, and function
• Drugs targeting the mitochondrion, especially antioxidants

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