Abstract
measured with sandwich-ELISA, using a commercial kit according to the manufacturer’s instructions (Millipore, Temecula, USA). The genotyping of BDNF val66met polymorphism was performed using 5′nuclease TaqMan allelic discrimination assay on the ABI 7500 Sequence Detection System (Applied Biosystems, Carlsbad, USA). Results: 25 (69.4%) patients out of 36 were female and the mean age was 37.8 (SD= 11.8) years. No differences in age, sex, ethnicity and serum BDNF levels were found between patients and controls (p = 0.807, p = 1.0, p = 0.710, and p = 0.075, respectively). Significant increase of serum BDNF levels was detected along the follow-up in depressive patients (F = 3.01, p = 0.49). After controlling for the polarity of episode and serum BDNF levels at baseline, serum BDNF levels were significantly higher in responders compared to non-responders (p = 0.005) as well as in remitters compared to non-remitters (p = 0.050). There was a significant negative correlation between differences in serum BDNF levels and in CGI score along the follow-up (r = −0.372, p = 0.028). Val66met polymorphism did not seem to be related to response to treatment. Conclusions: Changes in serum BDNF levels may help in supervising treatment response. A deeper understanding about the molecular determinants involved in BDNFsignaling cascades may provide means for monitoring treatment response and disease progression as well as for the development of novel agents for the treatment of BD.
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