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ISSN 1750-1911 10.2217/EPI.11.87 © 2011 Future Medicine Ltd Epigenomics (2011) 3(5), 537–538 537 Dysfunction to the brain’s serotonergic system is believed to be a primary factor in the pathogenesis of schizophrenia and bipolar disorder [1], two psychiatric diseases that make a significant contribution to the global burden of disease. Serotonin has many functions in the CNS, regulating synapse formation, neuronal growth, cognitive processes and mood. Several of the most effective antipsychotic drugs are known to bind to serotonin receptors in the brain [2], and alterations in serotonin receptor levels have been reported in many psychiatric disorders, including schizophrenia and bipolar disorder [3]. Polymorphisms in the genes encoding these receptors are considered good candidates for mediating susceptibility to psychosis, and they have been widely studied in genetic association studies [4]. Recently, increasing emphasis has been placed on the potential role of epigenetic dysfunction in the etiology of psychosis [5,6], and converging evidence suggests that epigenetic factors are important in the regulation of serotonin receptor gene expression [7–9]. Carrard et al. used a high resolution melting technique to investigate DNA methylation in the promoter of the serotonin receptor type-1A (5HTR1A) gene in peripheral blood leukocytes of patients diagnosed with schizophrenia and bipolar disorder, compared with healthy controls, reporting a small but significant increase in methylation in both patient groups [8]. Given that increased promoter DNA methylation is often inversely correlated with gene expression [10], the reported disease-associated increase in DNA methylation is consistent with previous studies reporting decreased 5HTR1A mRNA levels in these disorders [3]. Although an ana lysis of the 5HTR1A gene expression in the same samples would have further consolidated this association, it is of note that the reported hyper methylation is observed in both schizophrenia and bipolar disorder, a finding consistent with previous data, suggesting that they share common etiological factors [11]. Unfortunately, the high resolution melting method used in this study is unable to resolve allelespecific DNA methylation patterns at base-pair resolution and although blood is a useful tissue for observing epigenetic changes occurring during early embryogenesis, the authors note that it would be optimal to replicate these data in a disease-relevant tissue (i.e., the brain), given the tissue-specific nature of the epigenome. It is also plausible that the blood cells studied here are liable to DNA methylation changes resulting from factors associated with the disease itself (e.g., medication exposure), making conclusions about the causal nature of the observed differences difficult. Research Highlights

Research Highlights: Epigenetic changes to serotonin receptor gene expression in schizophrenia and bipolar disorder