Bipolar disorder is an episodic sickness characterized by depression and periodic mood elevation. The etiopathology of bipolar disorder is linked to environmental factors that exert stress on brain function via epigenetic influence, particularly DNA methylation and histone proteins modifications (Schmitt, Malchow, Hasan, & Falkai, 2014). Studies have shown discrepancies in methylation of GPR24 and CTNNA2 genes, which are implicated in psychosis. Maternal and paternal methylation of X-allele has been implicated as the cause of discordance in BPD in twins. Studies of epigenetics of neurotransmission have attributed the hypermethylation of SLC6A4 gene in BPD lymphoblastoid cells of bipolar individuals at two CpG sites. The hypermethylation of SLC6A4 is correlated with SLC6A4 mRNA levels in individuals with S/S genotype of HTTLPR who have less expression suggesting that environmental factors play a partial role in the pathophysiology of BPD (Kang et al., 2013). Serotonin receptor subtype 1A (5HTR1A) found in the cortico-limbic regions of the brain has a high epigenetic alteration in BPD individuals leading to altered neurotransmitter binding (Teroganova et al., 2016). There is an increase in methylation of genes encoding 5HTR1A in the brain of a bipolar individual. Genome-wide studies have revealed important hypomethylation of CpG island of human leukocyte antigen 9 gene (HCG9) in bipolar patients. This gene is found on chromosome 6, which is associated with bipolar disorder (Kaminsky et al., 2012).
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