title: Effect of amyloid precursor protein 17mer peptide on microtubule structure and tau protein hyperphosphorylation in hippocampal neurons of experimental diabetic mice.
abstract: The objective of this study was to investigate whether microtubular structure changes and tau protein hyperphosphorylation exist in hippocampal neurons of experimental diabetic mice, and to study the effect of amyloid precursor protein 17mer peptide. The results showed that the microtubules of hippocampal neurons of diabetic mice manifested prominent signs of fragmentation and dissolution, tau protein is hyperphosphorylated at Ser 199/Thr 202 sites, enzymes related to the phosphorylation and dephosphorylation of tau protein were diminished. The administration of amyloid precursor protein 17mer peptide could ameliorate the foregoing changes in diabetic mice. These results indicated that protein synthesis in the brain tissue of diabetic mice decreased. Amyloid precursor protein 17mer peptide acted as a neuroprotective agent that globally alleviates the disturbances due to impaired energy metabolism in diabetic mice.
authors.affiliation: Beijing Research Laboratory or Brain Aging, Xuan-Wu Hosptial, Capital University of Medical Sciences, China.
authors.forename: Yong-Mei
authors.initials: YM
authors.lastname: Zhao
authors.forename: Jin-Jing
authors.initials: JJ
authors.lastname: Pei
authors.forename: Zhi-Juan
authors.initials: ZJ
authors.lastname: Ji
authors.forename: Zhi-Wei
authors.initials: ZW
authors.lastname: Zhao
authors.forename: Yu-Ying
authors.initials: YY
authors.lastname: Qian
authors.forename: Shu-Li
authors.initials: SL
authors.lastname: Sheng
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D003072:Cognition Disorders / Q000209:etiology / Q000517:prevention & control; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000523:psychology; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D008870:Microtubules / Q000187:drug effects* / Q000648:ultrastructure; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D010446:Peptide Fragments / Q000494:pharmacology* / Q000627:therapeutic use; D010766:Phosphorylation / Q000187:drug effects; D011499:Protein Processing, Post-Translational / Q000187:drug effects*; D013311:Streptozocin; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016564:Amyloid beta-Protein Precursor; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C446879:amyloid beta-protein precursor 695 (319-339); D016875:tau Proteins; D013311:Streptozocin