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P3–435: Inhibition of protein phosphatases induces impairment in axonal transport and spatial memory retention
Author(s) -
Yang Ying,
Yang Xifei,
Tian Qing,
Wang Xiaochuan,
Li Hong-Lian,
Wang Qun,
Wang Jianzhi
Publication year - 2006
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.2006.05.1706
Subject(s) - hyperphosphorylation , neurofilament , axoplasmic transport , phosphatase , hippocampus , cytoskeleton , microbiology and biotechnology , neuroscience , hippocampal formation , tau protein , chemistry , western blot , morris water navigation task , biology , phosphorylation , alzheimer's disease , medicine , biochemistry , immunohistochemistry , immunology , cell , disease , gene
observed spines) resulting in no net change in spine density; however in aged Tg2576 mice, this balance is disrupted. Spine elimination is increased 3 fold in these mice to almost 15%, while spine formation remains normal, resulting in the observed net loss of spines. These effects are exacerbated near plaques. Conclusions: Together, these data imply that dense-cored amyloid plaques have a synaptotoxic effect resulting in altered structural plasticity. Supported by: NIH grants AG08487, AG00277, and Alzheimer’s Association Pioneer Award EB00768.