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Parkinson’s disease (PD), a devastating neurodegenerative condition, is becoming increasingly prevalent in our aging population, yet the events leading to neuron death remain unclear. Current treatments aim to alleviate symptoms, but none address the cause of neurodegeneration, leaving a cure for PD elusive. Disease progression is marked by significant neuron loss in the brain region responsible for mobility, caused by oxidative damage to the neurons’ energy-producing mitochondria. During oxidative stress in PD, the enzyme parkin prevents cell death and neuron loss. However, the structure of parkin is inherently vulnerable to oxidation, and its protective role in PD requires recruitment to a highly oxidizing environment. The objective of this research is to determine the mechanism and consequences of parkin oxidation at the molecular and cellular levels. Understanding parkin oxidation in relation to its neuroprotective activity is essential for identifying the events that link oxidative stress to the death of motor neurons. This groundwork has the potential to advance the development of new and effective PD treatments aiming to slow neurodegeneration. In partnership with Parkinson Society Southwestern Ontario, this work aims to boost community awareness of scientific findings and provide an underserved population with educational resources to strengthen support systems.
Gary Shaw;Martin Duennwald
Parkinson Society Southwestern Ontario
Life Sciences
Other services (except public administration)
The University of Western Ontario
Accelerate
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