Modulation of Mitochondrial Physiology in Neuroprotection and Neurotoxicity

Dear Colleagues,

Mitochondria are central to the production of adenosine triphosphate (ATP) in nucleated human cells. Moreover, these organelles are a major source of reactive species, mainly due to the presence of the oxidative phosphorylation (OXPHOS) system. The structure and number of mitochondria vary according to the cells’ needs. During human development, mitochondria are required to meet the energetic status of growing cells. Mitochondria also control cell death by apoptosis, which is important for tissues to acquire their mature structure. After completion of the growth phase, mitochondria are still necessary for maintaining cellular health in different ways. Certain stimuli, such as different types of stress, lead to cell adaptation involving mitochondrial responses that are not just limited to the production of ATP. In cells undergoing different types of stress, mitochondrial biogenesis may be required to improve both bioenergetic and redox states. Furthermore, modulation of mitochondrial dynamics (i.e., fusion and fission) may be observed as part of the response to stress, or as a negative consequence resulting from that event. Failure to adapt to stress favors the onset of cellular dysfunction and disease. In neurodegenerative disorders, for example, mitochondrial dysfunction results in bioenergetic collapse, redox impairment, and cell death by various mechanisms. Mitochondrial disorders may also be related to alterations in the function of other organelles, such as peroxisomes and endoplasmic reticulum. This indicates the presence of intricate relationships between different components of human cells during both physiological and pathological conditions. Strategies now exist to prevent and treat mitochondrial disturbances, such as those involving natural or synthetic molecules. Hence, this topic focuses on studies that demonstrate a role for mitochondria in maintaining the health of brain cells, as well as on the effects of modulating mitochondrial physiology on neuroprotection and neurotoxicity. We welcome original research reports, review articles, and perspectives in all areas relating to this topic.

Prof. Dr. Marcos Roberto de Oliveira

Guest Editor

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