The aim is to establish if glucosamine administration reduces the levels of Tau phosphorylation in an animal model of permanent ischemia.

Thrombolysis and thrombectomy) are the main treatments for stroke. However, a significant number of patients are not eligible for these treatments. Alternative managements are necessary to reduce post-stroke consequences (PSC). The aggregation of hyperphosphorylated Tau (P-Tau) is observed after brain ischemia which leads to PSC. Glucosamine has demonstrated positive effects on stroke and controversial effects over Tau. 

O-GlcNAcylation after stroke is protective against brain injury in reperfusion. However, permanent ischemia leads to irreversible changes including Tau hyperphosphorylation which could decrease the neuroprotective effects of O-GlcNAcylation. Glucosamine increased O-GlcNAcylation and P-Tau in our study (a paradoxical reaction). Nonetheless, the glucosamine group had less cell destruction what it may implies that glucosamine exerts neuroprotective effects by other mechanisms. Further investigations are needed.