Role of mitochondrial <scp>ROS</scp> in the brain: from physiology to neurodegeneration

<jats:p>Mitochondria are key cell organelles in that they are responsible for energy production and control many processes from signalling to cell death. The function of the mitochondrial electron transport chain is coupled with the production of reactive oxygen species (<jats:styled-content style="fixed-case">ROS</jats:styled-content>) in the form of superoxide anion or hydrogen peroxide. As a result of the constant production of <jats:styled-content style="fixed-case">ROS</jats:styled-content>, mitochondria are protected by highly efficient antioxidant systems. The rapidly changing levels of <jats:styled-content style="fixed-case">ROS</jats:styled-content> in mitochondria, coupled with multiple essential cellular functions, make <jats:styled-content style="fixed-case">ROS</jats:styled-content> apt for physiological signalling. Thus, mutations, environmental toxins and chronic ischaemic conditions could affect the mitochondrial redox balance and lead to the development of pathology. In long‐living and non‐mitotic cells such as neurons, oxidative stress induced by overproduction of mitochondrial <jats:styled-content style="fixed-case">ROS</jats:styled-content> or impairment of the antioxidant defence results in a dysfunction of mitochondria and initiation of the cell death cascade. Mitochondrial <jats:styled-content style="fixed-case">ROS</jats:styled-content> overproduction and changes in mitochondrial redox homeostasis have been shown to be involved in both a number of neurological conditions and a majority of neurodegenerative diseases. Here, we summarise the involvement of mitochondrial <jats:styled-content style="fixed-case">ROS</jats:styled-content> in the mechanism of neuronal loss of major neurodegenerative disorders.</jats:p>