Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10455001 | Brain, Behavior, and Immunity | 2009 | 11 Pages |
Abstract
Evidence has been gathered to suggest that trace amounts of copper induce neurotoxicity by interaction with elevated cholesterol in diet. Step-through task and Morris water maze task were used to evaluate cognitive function in the animals. Although a 16-week copper treatment alone in mice showed no significant change in learning and memory performances, cholesterol treatment significantly induced learning and memory impairments, which could be exacerbated by the co-treatment with copper. Immunohistochemical studies revealed that trace amounts of copper further stimulated the amyloid precursor protein (APP) upregulation and contributed to amyloid β-peptide (Aβ) deposition in the brain of cholesterol-fed mice. Western blot analysis showed that copper also increased the protein expression levels of tumor necrosis factor-α (TNF-α) and the degradation of IκB proteins in the brain of cholesterol-fed mice. Furthermore, increased production of high inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions were detected in the hippocampus and cerebral cortex of copper and cholesterol co-treated mice by immunohistochemical analysis. These findings suggest that trace amounts of copper could induce APP upregulation, activate inflammatory pathway and exacerbate neurotoxicity in cholesterol-fed mice.
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Authors
Jun Lu, Dong-mei Wu, Yuan-lin Zheng, Dong-xu Sun, Bin Hu, Qun Shan, Zi-feng Zhang, Shao-hua Fan,