Learned information, even episodic memory, can persist for a lifetime, as compared to proteins and mRNA within the activated neurons that subserve plasticity and memory formation, which are usually degraded in less than 24 hours. Recently, epigenetic marks, in particular DNA methylation, have emerged as key actors in memory maintenance.  Using Methylated DNA Binding Domain sequencing (MBD-seq), we show that DNA methylation is dynamically regulated genome-wide during learning and is disrupted in a mouse model for the learning disability Pitt-Hopkins Syndrome.  Moreover, the discovery that Vorinostat (SAHA) ameliorates the learning and memory deficits characterized in the Pitt-Hopkins Syndrome model suggests a central role of epigenetic mechanisms in the underlying chemistry of Pitt-Hopkins, potential therapeutic targets, and cognition in general.

Dynamic DNA methylation is essential for memory formation

247th National Meeting (2014)

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