Cornel iridoid glycoside protected synaptic function by inhibiting tau hyperphosphorylation

[Speaker] Lan Zhang:1
1:Xuanwu Hospital of Capital Medical University, China

Microtubule-associated tau protein is a pathological hallmark in Alzheimer's disease (AD), where hyperphosphorylation of tau generates neurofibrillary tangles. Recent reports underline that tau may be localized within both pre- and post-synaptic compartments, suggesting that it may possibly induce or contribute to synaptic dysfunction. P301L transgenic (tg) mice well mimic features of human tauopathies and provide a good model for investigating the role of tau in neurodegenerative events. The aim of the present study was to investigate the effect of cornel iridoid glycoside (CIG) on tau hyperphosphorylation and synaptic dysfunction.
Intragastric administration of CIG (100, 200mg/kg) could decrease hyperphosphorylated tau. In addition, p-tau correlated with a significant reduction of post-synaptic markers, such as GluN2A, GluN2B, GluA1, GluA2, syntaxin and PSD-95 in P301L mice. CIG increased the level of GluN2B, GluA1, GluA2, and syntaxin in P301L mice. The results demonstrated CIG protected synaptic function by inhibiting tau hyperphosphorylation. Taken together, these results suggest that CIG may be a potential new candidate for the treatment of AD and other tauopathies.

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