β-amyloid (Aβ) and copper play important roles in the pathogenesis of Alzheimer's disease (AD). However, the behavioral correlativity and molecular mechanisms of Aβ and copper toxicity have been investigated less often. In the present study, we investigated the interaction and toxicity of Aβ1-42 and copper in the Aβ1-42 transgenic Caenorhabditis elegans worm model CL2006.
View Article and Find Full Text PDFNicotine reduces beta-amyloidosis and has a beneficial effect against Alzheimer's disease (AD), but the underlying mechanism is not clear. The abnormal interactions of beta-amyloid (Abeta) with metal ions such as copper and zinc are implicated in the process of Abeta deposition in AD brains. In the present study, we investigated the effect of nicotine on metal homeostasis in the hippocampus and cortex of APP(V717I) (London mutant form of APP) transgenic mice.
View Article and Find Full Text PDFZhonghua Yu Fang Yi Xue Za Zhi
January 2005
Objective: To investigate the changing of T4 5'-and 5-deiodinase within rat brain under various iodin-nutritional states.
Methods: Animal model of iodine-deficiency rat was performed and the rats were divided into 4 groups by the intake of iodine-nutrition, and then killed at an age of 20 days. The thyroid hormones level in serum was measured by ELISA and the activity of T(4) 5'-and 5-deiodinase within brain was analyzed.
Oxidative stress is considered to be a mechanism involved in lead neurotoxicity. Apoptosis is also thought to relate to lead neurotoxicity. The present study, focused on the hippocampus, was designed to investigate the two possible mechanisms involved in lead neurotoxicity and the potential protective effects of 2,3-dimercaptosuccinic acid (DMSA) and oligomeric procyanidins (OPC).
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