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P2‐159: Melatonin meliorates calyculin A‐induced axonal transport defects and spatial memory retention impairment in rats
Author(s) -
Yang Ying,
Yang Xifei,
Tian Qing,
Wang Qun,
Wang Jianzhi
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1233
Subject(s) - axon , melatonin , neurofilament , morris water navigation task , hyperphosphorylation , tau protein , hippocampus , axoplasmic transport , neuroscience , memory impairment , chemistry , medicine , endocrinology , biology , microbiology and biotechnology , phosphorylation , alzheimer's disease , cognition , immunohistochemistry , disease
wild type mice. Meanwhile, we further detected the alterations in Aktglycogen synthase kinase (GSK)-3 signaling associated with oxidative stress and found decreased phosphorylation of both Akt and GSK-3 in the transgenic mice. Concurrently, we detected an increased oxidative stress reaction as evidenced by elevated level of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) in hippocampus of the transgenic mice. In addition, exogenous supplementation of antioxidant coenzyme Q10 (CoQ10) not only partially decreased MDA level and up-regulated the activity of SOD, but also attenuated tau hyperphosphorylation, concurrently accompanied with a restoration of Akt-GSK-3 signaling. Conclusions: These results suggest that tau hyperphosphorylation is associated with enhanced oxidative stress and the mechanisms may involve oxidative stress-mediated depression of Akt-GSK-3 signaling. The neuroprotective effect of CoQ10 could be attributed to its antioxidant property. Our data indicate that CoQ10 might be a potential therapeutic candidate in AD treatment.