A chromatin-modifying enzyme impairs memory formation in mice, a Nature paper reveals. Histone deacetylases catalyse the removal of acetyl groups from histones, the main protein component of chromatin. Drugs that selectively block the enzyme's activity may prove useful in human diseases in which memory is impaired.
Boosting levels of histone deacetylase 2 (HDAC2) in neurons impairs learning and memory in mice, Li-Huei Tsai and colleagues show, whereas boosting levels of a related enzyme, HDAC1, does not. In line with this, when HDAC2 is boosted, several markers of learning and memory, such as dendritic spine number, synapse density and plasticity, are reduced. In contrast, reducing expression of HDAC2 had the opposite effects on memory formation and its cellular correlates. Further work revealed that HDAC2 specifically associates with genes believed to be involved in plasticity and memory, whereas HDAC1 does not.
These studies will spur on drug-development strategies better-targeting HDAC2 instead of HDAC1, potentially enhancing the treatment of human diseases associated with memory impairment.
Li-Huei Tsai (Massachusetts Institute of Technology, Cambridge, MA, USA)
(C) Nature press release.
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