O4‐05‐02: Tau‐induced defects in hippocampal neuroplasticity, learning and memory are reversible in a regulatable transgenic mouse model

Phosphorylation in two discrete tau domains regulates a stepwise process leading to postsynaptic dysfunction

“…The long-lasting synaptic plasticity defects that are associated with neurological disorders commonly feature a dysregulation of glutamatergic AMPA receptors in the postsynaptic membrane of dendritic spines (Hoover et al 2010;Ittner et al 2010;Kam et al 2010;Miller et al 2014;Zhao et al 2016). Recently, reports have linked soluble, post-translationally modified forms of tau, either directly or indirectly, to defects in AMPA receptor trafficking (Hoover et al 2010;Sydow et al 2011). Some of the post-translational modifications that have been described are phosphorylation by proline-directed kinases (Hoover et al 2010), cleavage by caspase-2 (Zhao et al 2016), and acetylation by major tau acetyltransferases p300 and CREB-binding protein (CBP) (Min et al 2010;Tracy et al 2016).…”