A quantitative approach towards the characterisation of mitochondrial dysfunction in Parkinson’s disease
Mitochondrial dysfunction is implicated in Parkinson’s Disease (PD), but detailed understanding of the cause and effect in αSyn toxicity is lacking. Through provision of quantitative and systematic characterisation of mitochondrial dysfunction, PD-MitoQUANT will provide unprecedented understanding of the role of mitochondrial dysfunction in PD, identify and validate novel disease biomarkers, and propose innovative therapeutic targets that can be further progressed by the EFPIA partners. The consortium leverages multi-disciplinary expertise in the fields of αSyn biochemistry, iPSC-derived PD models, mitochondrial function and structural analysis, proteotoxicity, ER stress and UPR signaling, systems biology of mitochondrial function, and in vivo animal models. A key focus will be quantitative description and integrated analysis of mitochondrial function and its relation to proteotoxicity; representing a key panel of consortium partners Prehn [RCSI], Abramov [UCL], Corti [ICM] and Koopmann [RUMC] who also have assembled long–standing expertise in primary neuron culture, iPSC-derived neurons, PD in vivo models, proteostasis and ageing studies.
It is geneXplain’s role in this consortium to apply its proprietary methodology of computational upstream analysis and master regulator search to the data generated by the project partners.