| Literature DB >> 26050140 |
Benjamin Dehay1, Mathieu Bourdenx1, Philippe Gorry2, Serge Przedborski3, Miquel Vila4,5,6, Stephane Hunot7,8,9,10, Andrew Singleton11, C Warren Olanow12, Kalpana M Merchant13, Erwan Bezard1, Gregory A Petsko14, Wassilios G Meissner1.
Abstract
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.Entities:
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Year: 2015 PMID： 26050140 PMCID： PMC5217462 DOI： 10.1016/S1474-4422(15)00006-X
Source DB: PubMed Journal: Lancet Neurol ISSN： 1474-4422 Impact factor: 44.182