Article ID Journal Published Year Pages File Type
10455001 Brain, Behavior, and Immunity 2009 11 Pages PDF
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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