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PD-MitoQUANT – A quantitative approach towards the characterisation of mitochondrial dysfunction in Parkinson's disease

Project description

Role of proteotoxicity in mitochondrial dysfunction linked to Parkinson's disease

Alpha-synuclein (αSyn) aggregates form insoluble fibrils in pathological conditions such as Parkinson's disease (PD). Mitochondrial dysfunction is implicated in PD, but a detailed understanding of the cause and effect of αSyn toxicity is lacking. The EU-funded PD-MitoQUANT project aims to elucidate the role of mitochondrial dysfunction in PD, identify and validate novel disease biomarkers and propose innovative therapeutic targets. The project consortium includes partners from academia and industry with multidisciplinary expertise in the fields of αSyn biochemistry, stem cell-derived PD models, mitochondrial function and structural analysis, mitochondrial function systems biology and in vivo animal models. The project is focussing on a quantitative description and integrated analysis of mitochondrial function and its relation to proteotoxicity.

Objective

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. These investigations will be supported by expert teams in iPSC-derived in vitro PD models and in vivo PD models from the academic partners (Hunot [ICM], Melki [CNRS], Di Monte [DZNE], Broccoli [CNR], SME [Mimetas] and EFPIA partners [Teva], [Lundbeck] and [UCB]. Through integrated in vitro, in silico and in vivo approaches, and supported computationally by SME [GENEXPLAIN], PD-MitoQUANT will perform thorough and unprecedented investigations of mitochondrial dysfunction. Finally, the consortium will initiate a European research platform of excellence investigating mitochondrial dysfunction in PD continuing beyond the project, further supported by [PUK]’s PD human tissue biobank. This will provide long-term and sustainable progress in the understanding of mitochondrial dysfunction in PD and towards clinical application.

Coordinator

ROYAL COLLEGE OF SURGEONS IN IRELAND
Net EU contribution
€ 1 088 108,20
Address
ST STEPHEN'S GREEN 123
2 Dublin
Ireland

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Region
Ireland Northern and Western Border
Activity type
Higher or Secondary Education Establishments
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Total cost
€ 1 088 108,20

Participants (14)