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Can Parkin and PINK1 protect against neurodegeneration in vivo?

BACKGROUND AND HYPOTHESES: PD is a mitochondrial disorder characterized by dysfunctional mitochondria, oxidative stress, neuroinflammation, protein inclusions and degeneration of midbrain dopaminergic neurons. Plant atioxidants can prevent inflammation an d the accumulation of ROS. I hypothesize that a diet rich in antioxidants can increase the neuron's ability to protect themselves against oxidative stress, and thus decelerate PD progression. Possibly, regulation of the PARK1-parkin pathway of mitophagy i s one mechanism by which antioxidants exert their protective actionMAIN OBJECTIVES AND METHODS: I will use gentic mouse models for PD to elucidate the effects of antioxidants on hallmarks of the disease. I will perform behavioral- and pathoanatomical ex aminations. By use of light- and confocal microscopy, I will investigate the degree of neurodegeneration, activity of some enzymes that are important for the red-ox state of the cells, activation of microglia and protein inclusions typical of PD. I will u se electron microscopy to investigate whether the dysfunctional mitochondria of these animals display abnormal morphology or appear to escape from autophagy. I will treat the PD animal models with a diet rich in antioxidants, and use the methods described above to investigate whether antioxidants can decelerate disease progression in PD.

Prosjektleder:
Cecilie Morland
Institusjon:
UoH-sektor/Universitetet i Oslo/Det medisinske fakultet
Aktivitetsnavn:
Mobilitet Norge-USA Canada
Prosjektstatus:
Bevilgning
Prosjektperiode:
01.07.2013 - 30.06.2014
Geografi:
Norge/OSLO
Fagområder:
Medisinske fag/Klinisk medisinske fag/Nevrologi
Prosjektnummer:
225344