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We searched PubMed, Medline, Cochrane Library, reference lists of relevant studies to June 2012, and email contact with authors. For the case-control studies, the authors found 1) support for the association between PD and GBA, both in total group analysis [fixed: OR and 95%CI: 4.825 Selleck MAPK Inhibitor Library (3.901�C5.968), P?Selleck Metformin over the age of 65 years and more than 4% of the population over 85 years [de Rijk et al., 2000; Zhang et al., 2005]. Although the exact etiology of PD is not currently fully understood, more and more evidence suggested that environment, genetic factors and progress of aging had essential influences on the pathogenic mechanism Alkannin of this disease. In the last several decades, insights in genetic characteristics of PD have dramatically increased. Genetic studies from different geographical regions worldwide have strengthened the hypothesis that PD has a substantial genetic component [Gasser et al., 2011]. And a number of genes influence PD susceptibility has been identified [Bekris et al., 2010]. Recently, mutations in the glucocerebrosidase (GBA) gene were identified as risk factors for PD [Sidransky et al., 2009; Alcalay et al., 2012]. The human GBA gene, mapped on chromosome 1q21-22, is comprised of 11 exons encoding a 497 amino acid enzyme with glucosylceramidase activity, which is needed to cleave, by hydrolysis, the beta-glucosidic linkage of the chemical glucocerebroside, an intermediate in glycolipid metabolism. This enzyme is active in lysosomes, which are structures inside cells that act as recycling centers. Deficiency of this enzyme leads to the impairment of glucosylceramide degradation which causing the autosomal, recessively-inherited lysosomal storage disorder, Gaucher disease.