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001 Genetics of parkinsonism
N. Wood.Institute of Neurology, University of London, London, UK
Parkinson’s disease (PD) is a common and incurable neurodegenerative disease. The genetic bases of genetically “simple” forms of PD is rapidly being solve. In the last few years, five genes have been unequivocally shown to cause PD. These are α-synuclein, Parkin, LRRK2, PINK1 and DJ-1. It is now clear that nigral cell loss and the specific clinical and pathological phenotypes seen in PD can arise through a number of different genetic (and presumably molecular) mechanisms. What is much less clear is whether there are several independent pathways or whether there is convergence of the molecular events. The finding of such genetic factors provides a very solid base from which to work to form towards a deeper understanding of the causes of cell dysfunction and death. Complete knowledge of these gene functions remains elusive. Recent work implicates abnormal protein accumulation, mitochondrial dysfunction and oxidative stress as common pathways to PD pathology. Combined proteomic, cellular and in vivo modelling is required to generate and investigate these pathways but the ultimate and most difficult task is to show the relevance of these events in human disease.
002 NEW TREATMENTS FOR PARKINSON’S DISEASE
C. E. Clarke.University of Birmingham, Birmingham, UK
This presentation uses an evidenced based approach to summarise recent developments in the drug treatment of Parkinson’s disease (PD) with emphasis on new agents and novel administration routes. This will include some non-motor features such as dementia and psychosis.
Rotigotine is a non-ergot dopamine agonist. It is lipid soluble and therefore it has been developed as a transdermal delivery system (patch) which produces stable 24 h stimulation from one application. Continuous dopaminergic stimulation may prevent or reverse motor complications. Rotigotine has been shown to be effective in two phase 2 and 3 placebo controlled trials. One phase 3 trial …
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