Journal
CELLULAR AND MOLECULAR NEUROBIOLOGY
Volume 34, Issue 6, Pages 805-812Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-013-0012-y
Keywords
Alzheimer's disease; Histone deacetylase; Memory; Valproic acid; Synaptic plasticity
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Funding
- Doctorial Innovation Fund of Peking Union Medical College [2010-1001-001]
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Alzheimer's disease (AD) is a very common progressive neurodegenerative disorder affecting the learning and memory abilities in the brain. Key findings from recent studies of epigenetic mechanisms of memory suggest chromatin remodeling disorders via histone hypoacetylation of the lysine residue contribute to the cognitive impairment in AD. Therefore, the deinhibition of histone acetylation induced by histone deacetylases (HDACs) inhibitors contributes to recovery of learning and memory. We show here that the antiepileptic drug sodium valproate (VPA) potently enhanced long-term recognition memory and spatial learning and memory in AD transgenic mice. Possible mechanisms showed VPA could significantly elevate histone acetylation through HDACs activity inhibition and increase plasticity-associated gene expression within the hippocampi of mice. Our study suggests that VPA, serving as a HDACs inhibitor, can be considered as a potential pharmaceutical agent for the improvement of cognitive function in AD.
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