Published online by Cambridge University Press: 24 June 2014
Lee H-Y, Kim Y-K. Effect of TGF-β1 polymorphism on the susceptibility to schizophrenia and treatment response to atypical antipsychotic agent.
Several studies have suggested that cytokine alterations could be related to the pathophysiology of schizophrenia. Transforming growth factor-beta1 (TGF-β1) is believed to be an important factor in regulation of inflammatory responses and to have anti-inflammatory effects. TGF-β1 also has trophic effects on dopaminergic neurons. We tested the hypothesis TGF-β1 is associated with the pathophysiology of schizophrenia.
The polymorphisms at codon 10 (T869C) and codon 25 (G915C) of TGF-β1 were analysed in 99 schizophrenia patients and 130 normal controls. At baseline and after 8 weeks of treatment, clinical symptoms were evaluated on Positive and Negative Syndrome Scale (PANSS).
None of the subjects were polymorphic at codon 25. However, the C allele at codon 10 was more frequent in schizophrenia (p = 0.05). Although schizophrenia group showed a higher tendency of allele frequency in the subjects with C allele (p = 0.05), the allelic difference did not reach statistical significance after correction for multiple comparisons (p = 0.1).
PANSS scores showed no significant correlation with genotypes. The genotype distribution was not significantly different between responders and non-responders. However, the C allele was more frequent among responders (p = 0.03).
These results suggest that the TGF-β1 polymorphism is associated with therapeutic response to antipsychotics. However, further studies with larger numbers of subjects are needed to confirm the effect of TGF-β1 in schizophrenia.