The paper that the Big Think article references is "Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer’s disease" which uses two small molecule inhibitors (BIX01294 and UNC0642) of euchromatic histone methyltransferases EHMT1 and EHMT2. They also performed RNA interference-mediated knockdown of EHMT1 and EHMT2 using lenti-viral vectors expression shRNAs against EHMT1 and EHMT2. Sorry narmac.....not BET inhibitors.

Here is a passage from the introduction of the paper that discusses histone lysine methylation:

"One epigenetic way to control gene expression is through chromatin remodelling, a process that dynamically modifies chromatin architecture to allow or prevent transcription machinery proteins to access condensed genomic DNA (Li et al., 2007; Borrelli et al., 2008). A key process to alter chromatin architecture is the addition and removal of methyl groups to histones controlled by a plethora of histone methyltransferases and demethylases, respectively (Greer and Shi, 2012). Lysine (K) residues on histone proteins can be mono-, di- or trimethylated by specific histone modifying enzymes, which is associated with gene activation or repression (Barski et al., 2007; Heintzman et al., 2007)."

Epigenetics is a broad term. This paper deals with histone lysine methylation. Most discussion of BET bromodomains deals with histones lysine acetylation. Both could be important, as evidenced by this paper "Altered histone acetylation is associated with age-dependent memory impairment in mice." 

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