Mitochondria are central to survival of brain cells as evident by the severe disorders caused by mutations of mitochondrial proteins, or by toxins targeting the electron transport system. Importantly, the energy-generating function of mitochondria relies entirely on an intact inner membrane. During cellular calcium overload and altered redox state mitochondria can undergo a rapid permeabilization of the inner membrane, the so-called mitochondrial permeability transition (mPT). The present research program is focused on the role of mitochondria in neurodegeneration. It includes characterization of mPT, its regulation and consequences for mitochondrial and cellular function such as loss of energetic function, production of radical oxygen species (ROS), release of stored calcium and apoptogenic factors and reversal of the ATP synthase (causing cellular energy depletion). We use classical as well as novel ultra-sensitive systems for analysis of mitochondrial function, ROS detection and calcium handling in mitochondria derived from rodent and human cells and tissues.
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Last modified: 2008-09-10