Could decitabine treatment impair memory functions in humans?

Abstract

The role of epigenetic mechanisms in cognitive functions and neurological/psychiatric disorders has been studied in a number of studies recently. One of these mechanisms is DNA methylation, for which DNA methyltransferases (DNMT) are responsible. Decitabine, or 5-aza-2'-deoxycytidine, is a cytosine-analog DNMT inhibitor and is used in the treatment of certain myelodysplastic syndromes (MDS) subsets. Several studies address the role of DNA methylation and negative effects of decitabine on memory formation and consolidation in animals. We, therefore, hypothesize that standard decitabine treatment for MDS in patients without dementia might cause learning and memory deficits. A clinical trial is proposed to test the hypothesis which could support the role of DNA methylation in cognitive abilities of humans.