| Literature DB >> 19021754 |
Jose Bras1, Andrew Singleton, Mark R Cookson, John Hardy.
Abstract
Heterozygous loss-of-function mutations at the glucosecerebrosidase locus have recently been shown to be a potent risk factor for Lewy body disease. Based on this observation, we have re-evaluated the likelihood that the different PARK loci (defined using clinical criteria for disease) may be misleading attempts to find common pathways to pathogenesis. Rather, we suggest, grouping the different loci which lead to different Lewy body disease may be more revealing. Doing this, we suggest that several of the genes involved in disparate Lewy body diseases impinge on ceramide metabolism and we suggest that this may be a common theme for pathogenesis.Entities:
Mesh:
Substances:
Year: 2008 PMID: 19021754 PMCID: PMC2646080 DOI: 10.1111/j.1742-4658.2008.06709.x
Source DB: PubMed Journal: FEBS J ISSN: 1742-464X Impact factor: 5.542