Mitochondria, cellular power plants, malfunction in Parkinson's disease (PD) and with advanced age. Aging and PD cause changes in communication between mitochondria and the rest of the cell, which prevents the elimination and replacement of malfunctioning mitochondria. Blocking faulty avenues of communication can preserve mitochondria function and slow PD progression.
We will examine how changes in mitochondria-cell communication contribute to PD, and evaluate the effectiveness of targeting changes in mitochondria-cell signaling as a therapeutic strategy in a pre-clinical model of PD.
We will identify PD-specific changes in mitochondria-cell communication by measuring protein levels on the mitochondrial outer membrane in a pre-clinical model of PD. We will then block a line of communication known to promote mitochondrial dysfunction and will evaluate its effectiveness in a pre-clinical model of PD.
Impact on Diagnosis/Treatment of Parkinson's Disease:
Additional research is needed to understand the connection between aging and PD. Identification of changes in mitochondrial outer membrane proteins may help develop biomarkers to measure disease progression and develop novel targets for drug discovery.
Next Steps for Development:
The successful completion of these studies will provide a complete set of changes that occur in mitochondria-cell communication and move toward clinical validation of therapeutic targets.