Research group leader
- Adjunct Professor, PhDLaura Kytövuori
- Professor Emeritus, NeurologyKari Majamaa
Research group description
The mechanisms involved in dopaminergic degeneration in Parkinson´s disease (PD) are not clearly understood. Identification of mutations in various genes has suggested that the pathogenesis of PD involves common mechanisms, such as endosomal protein sorting and recycling, synaptic transmission, mitochondrial maintenance and lysosome-mediated autophagy. Mitochondria are cell organelles that convert energy stored in organic molecules to ATP that can be used in a variety of cellular processes as an energy source. Mitochondrial Complex I activity has been found to be decreased in patients with PD and, interestingly, a toxin inducing parkinsonism in humans is a Complex I inhibitor. Identification of a clinically distinct form of PD with mitochondrial impairment would enable more precise definition of PD subtypes, targeted genetic testing, and provide new biomarkers associated with mitochondrial PD.
Where are we headed
We attempt to examine the role of mitochondrial aberration in patients with early-onset PD ascertained previously from the Finnish population as well as in patients with idiopathic PD ascertained from the population of North and East of Finland. Possible outcomes of this research would be more precise definition of PD subtypes, targeted genetic testing, and new biomarkers associated with mitochondrial PD.
Our main collaborators
- Andrew Singleton, NIH
- Mika Martikainen, University of Turku
How to find us
Research Unit of Clinical Medicine
Neurocenter at Oulu University Hospital
Clinical Research Center