Over the past years, fundamental and translational biomedical research have identified a wealth of disease-related molecular mechanisms. The contemporary knowledge, although still far from complete, has resulted in different approaches trying to correct the cellular consequences of mitochondrial dysfunction ranging from small molecules towards gene therapy. Research in my group studies the consequences of genetic and environmental mitochondrial failure at all level of complexities from single cell studies up to studies in patients and translates these observations into potential new intervention options. Current focus is on genetic defects of the oxidative phosphorylation system and genetic forms of Parkinson disease.
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