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Mitochondrial and lysosomal dysfunction in the pathogenesis of Parkinson’s disease
Published on December 2, 2014 35 min
Other Talks in the Series: Parkinson's Disease
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- Prof. Andre Parent
- Université Laval Quebec City, Quebec, Canada
Promising medical therapies for Parkinson’s disease
- Prof. Robert A. Hauser
- University of South Florida, USA
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- Prof. Michael S. Okun
- University of Florida, USA
Hello, my name is Tony Schapira. I'm going to talk to you today about mitochondrial and lysosomal dysfunction in the pathogenesis of Parkinson's disease. Parkinson's disease is a common disorder. Indeed, it is the second commonest neurodegenerative disorder after Alzheimer's disease. It's anticipated that the total number of people in the world with Parkinson's disease will double by 2030. This is a consequence of increased life expectancy of people, and reflects the increasing incidence of Parkinson's disease with age.
Several biochemical abnormalities have been associated with the pathogenesis of Parkinson's disease, and, of course, ultimately, with the etiology of this disorder; these include mitochondrial dysfunction, oxidative stress, intracellular calcium homeostasis, excitotoxicity, inflammation, protein misfolding, accumulation, aggregation, and, of course, now we know that this may also include abnormal propagation of proteins, apoptosis, and autophagy, which includes mitophagy, the turnover of mitochondria, and lysosomal dysfunction.
Today I'm going to focus on mitochondrial dysfunction and lysosomal dysfunction, as these are two very important areas of the pathogenesis of Parkinson's disease, and two which have attracted considerable attention over the past few years. Let me begin with the mitochondrial contribution to Parkinson's disease, and I'm first of all going to cover some basic mitochondrial biochemistry, so we can understand how abnormal mitochondrial function may contribute to the pathogenesis of Parkinson's disease.