B. Dehay, M. Bourdenx et al. in Lancet Neurol.
Le 10 juin 2015
Targeting α-synuclein for treatment of Parkinson’s disease: mechanistic and therapeutic considerations
Benjamin Dehay*, Mathieu Bourdenx*, Philippe Gorry, Serge Przedborski, Miquel Vila, Stéphane Hunot, Andrew Singleton, C Warren Olanow, Kalpana M Merchant, Erwan Bezard, Gregory A Petsko, Wassilios G Meissner
dans The Lancet Neurology (Published Online June 4, 2015 ; Impact Factor: 21.823) Review (Personal View)
Abstract PubMed :
Progressive neuronal cell loss in a small subset of brainstem and mesencephalic nuclei and widespread aggregation of the α-synuclein protein in the form of Lewy bodies and Lewy neurites are neuropathological hallmarks of Parkinson’s disease. Most cases occur sporadically, but mutations in several genes, including SNCA, which encodes α-synuclein, are associated with disease development. The discovery and development of therapeutic strategies to block cell death in Parkinson’s disease has been limited by a lack of understanding of the mechanisms driving neurodegeneration. However, increasing evidence of multiple pivotal roles of α-synuclein in the pathogenesis of Parkinson’s disease has led researchers to consider the therapeutic potential of several strategies aimed at reduction of α-synuclein toxicity. We critically assess the potential of experimental therapies targeting α-synuclein, and discuss steps that need to be taken for target validation and drug development.
Institute of Neurodegenerative Diseases, University of Bordeaux
Last update: 06.10.2015
Last update 05/04/18