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Epigenetic modification in the form of DNA methylation involves covalent addition of a methyl group from the methyl donor S adenosylmethionine to a cytosine base within the DNA. This reaction is catalyzed by a family of DNA methyltransferases (DNMTs), with DNMT1 and DNMT3A being the main enzymes in mammalian brain.14, 15, 16 DNA methylation in the promoter region of a gene has been associated with decreased transcriptional activity.17 CpG islands are extended regions of cytosine and guanine repeats in the promoter region of many mammalian genes. These sites are heavily targeted by DNMTs and are known to modulate gene expression.18Recently, we reported that AD and BD postmortem frontal cortex (Brodmann area 9) shows upregulation of mRNA and protein levels of neuroinflammatory and arachidonic acid (AA) cascade markers such as AA selective calcium independent cytosolic phospholipase A2 (cPLA2) IVA, secretory PLA2 (sPLA2 IIA and cyclooxygenase 2 (COX 2).1, 26 Loss of the synaptic proteins synaptophysin and drebrin is reported in both diseases,26, 27 and excitotoxicity is linked to increased glutamatergic function with loss of excitatory amino acid transporters in both disorders.28, 29 Brain derived neurotrophic factor (BDNF) also is reduced in the AD and BD brain.27, 30 The increased inflammatory and AA markers in BD are associated with increased mRNA and protein levels of transcriptional factor nuclear factor kappa B (NF subunits.2.
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