%0 Journal Article
%T Subcutaneous liraglutide ameliorates methylglyoxal-induced Alzheimer-like tau pathology and cognitive impairment by modulating tau hyperphosphorylation and glycogen synthase kinase-3¦Â
%A Libin Liu
%A Lijuan Wu
%A Linfang Ke
%A Liqin Qi
%A Xiaohong Liu
%A Xiaowei Lin
%A Xiaoying Liu
%A Yanping Wang
%A Yu Zhou
%A Zhongjie Zheng
%A Zhou Chen
%J Archive of "American Journal of Translational Research".
%D 2017
%X Memory deterioration and synapse damage with accumulation of ¦Â-amyloid and hyperphosphorylated tau are hallmark lesions of Alzheimer¡¯s disease (AD). Methylglyoxal (MG), a key intermediate of glucose metabolism, is elevated in AD brains and modifies A¦Â42, increasing misfolding and leading to the accumulation of senile plaques. Liraglutide, an analog of glucagon-like peptide-1 (GLP-1), is neurotrophic and neuroprotective. However, whether liraglutide can protect against AD-like memory-related deficits and tau hyperphosphorylation caused by MG in vivo is not known. Here, we report that MG induces tau hyperphosphorylation and causes ultrastructural hippocampal damage and cognitive impairment in C57BL/6J mice. Liraglutide reduced these effects via activation of the protein kinase B and glycogen synthase kinase-3¦Â pathways. Our data reveal that liraglutide may alleviate AD-like cognitive impairment by decreasing the phosphorylation of tau
%K Alzheimer¡¯s disease
%K methylglyoxal
%K glucagon-like peptide-1
%K glycogen synthase kinase-3¦Â
%K tau protein
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5340664/