Mitochondrial dysfunction and susceptibility to Parkinson’s disease: New models of pathogenetic interactions 

Donato A. Di Monte (DZNE), David S. Park (CIHR), Fabio Blandini (MDS), Anthony H.V. Schapira (MRC)

The scope of this project is to develop and use animal models that better mimic the complex interactions that underlie Parkinson’s disease (PD) development. Abnormalities in mitochondria, organelles responsible for the energy balance of the cell, are likely to play an important role in neuronal dysfunction and neurodegeneration in PD. Using animal models that feature neuronal mitochondrial impairment, we will determine how this deficiency acts together with other toxic mechanisms in promoting neurodegenerative processes. We will also study novel strategies that counteract mitochondria-mediated pathology and could ultimately lead to neuroprotective intervention in PD. 

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