Inhibition of lysine methyltransferase G9a/GLP reinstates long-term synaptic plasticityand synaptic tagging/capture by facilitatingprotein synthesis in the hippocampal CA1area of APP/PS1 mouse model ofAlzheimer’s disease

摘要

Histone H3 lysine 9 di-methylation(H3K9me2)is an epigenetic repressive histone modification that was found at aberrant states in Alzheimer’s disease(AD)patient samples[1].The addition of H3K9me2/3 is mainly catalyzed by lysine methyltransferase G9a,which functions as a heteromeric complex with G9a-like protein(GLP).G9a/GLP has other non-histone substrates,including itself.G9a/GLP is implicated in regulating synaptic plasticity,learning and memory[2,3].