Abstract
Disruptions of dendritic spines are reported for many CNS diseases and are closely related to cognitive impairment. In patients with Alzheimer’s disease (AD), synapse loss in the hippocampus is strongly correlated with cognitive deficits. There is a growing realization that epigenetic regulation through histone deacetylases (HDACs) play a role in synaptic function and plasticity. HDAC2 overexpression in mice has been shown to decrease spines, synapses and cause cognitive impairment; the opposite is observed in HDAC2 knockout mice. In addition, cognitive deficits have been shown to be attenuated following treatment with HDAC inhibitors.
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