Mitochondrial dysfunction and energy deprivation in the mechanism of neurodegeneration

  • 1 Department of Clinical and Movement Neurosciences, UCL Institute of Neurology, Queen Square, London WC1N 3 BG, UK
  • 2 Department of Pathophysiology, Sechenov First Moscow State Medical University, Trubetskaya str., 8, 119048 Moscow, Russia
Andrey Y. AbramovORCID iD: https://orcid.org/0000-0002-7646-7235 and Plamena R. Angelova
  • Corresponding author
  • Department of Clinical and Movement Neurosciences, UCL Institute of Neurology, Queen Square, London WC1N 3 BG, UK
  • Department of Pathophysiology, Sechenov First Moscow State Medical University, Trubetskaya str., 8, 119048 Moscow, Russia
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Abstract

Energy-producing organelles mitochondria are involved in a number of cellular functions. Deregulation of mitochondrial function due to mutations or effects of mitochondrial toxins is proven to be a trigger for diverse pathologies, including neurodegenerative disorders. Despite the extensive research done in the last decades, the mechanisms by which mitochondrial dysfunction leads to neuronal deregulation and cell death have not yet been fully elucidated. Brain cells are specifically dependent on mitochondria due to their high energy demands to maintain neuronal ion gradients and signal transduction, and also, to mediate neuronal health through the processes of mitochondrial calcium homeostasis, mitophagy, mitochondrial reactive oxygen species production and mitochondrial dynamics. Some of these processes have been independently implicated in the mechanism of neuronal loss in neurodegeneration. Moreover, it is increasingly recognised that these processes are interdependent and interact within the mitochondria to ensure proper neuronal function and survival.

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