2007). In addition, PIK3C3 is located on chromosome 18q12.3, within the region that maps closely to markers D18S450 and D18S487, linked to SZ (Williams et al. 1999). The implication of genetic factors in SZ and bipolar disorder (BD) is now well established (Craddock et al. 2006). Unsurprisingly, associations between PIK3C3 gene variants in SZ and BD have been reported (Stopkova et al. 2004; Duan et al. 2005; Saito et al. 2005). These studies suggested that PIK3C3 is a putative candidate gene for SZ, BP, and other neurodevelopmental diseases. Brain-derived neurotrophic factor
Inhibitors,research,lifescience,medical (BDNF) is a member of the neurotrophin family, also known for its role in neurodevelopment and cell survival (Huang and Reichardt 2001). A number of studies have indicated that BDNF is implicated in major depression, mood disorder, and SZ (Duman 2005; Karege et al. 2002; Lu and Martinowitch 2008).
Several studies Inhibitors,research,lifescience,medical have subsequently reported some BDNF gene polymorphisms associated with mood disorder and psychosis, particularly the rs6265 (A196G), which replaces a valine by a methionine residue Inhibitors,research,lifescience,medical at position 66 of the protein (Neves–Pereira et al. 2002; De Luca et al. 2008; Vincze et al. 2008) although others failed to replicate this association (Tochigi et al. 2006; Watanabe et al. 2006). Lastly, basic studies have shown functional interactions between the neurotrophins—BDNF or neurotrophin-3 (NT-3)—and the phosphoinositol-3 kinase signaling pathway (Kaplan and Cooper 2001; Simpson et al. 2003; Reichardt 2006). In this study, we aimed to replicate the association between the PIK3C3 promoter variant, rs3813065, in both SZ and BP. This SNP Inhibitors,research,lifescience,medical is located in a crucial Inhibitors,research,lifescience,medical promoter area that could control the
expression of this gene by POU-containing transcription factors (Stopkova et al. 2004). Additionally, we tested two single nucleotide polymorphisms (SNPs) and assessed their allelic and haplotype associations: rs8095411 and a dinucleotide repeat (CA) polymorphism Entinostat also located upstream, PIK3C3. In a second time, we assessed the putative genetic interaction between PIK3C3 and BDNF in both disorders. Finally, we evaluated the overlap hypothesis between SZ and BD by highlighting genetic variants in common for these diseases (Craddock et al. 2006). Given the central place occupied by PI3K and BDNF proteins in signaling networks and their crucial role in neurodevelopment and synaptic plasticity, we aim to determine whether these two disorders show similar patterns of genetic association. Materials and Methods Subjects Patients meeting DSM-IV criteria for BD (N = 98) or SZ (N = 79) and controls (N = 158) were included after they had given informed consent and approval of ethics committee had been obtained (Table 1).
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