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Review Copper in Alzheimer's disease: too much or too little? 2009
Quinn JF, Crane S, Harris C, Wadsworth TL. · Oregon Health and Science University, Portland VA Medical Center, Department of Neurology, Portland, OR 97239, USA. · Expert Rev Neurother. · Pubmed #19402774 No free full text.
Abstract: A considerable amount of literature has accrued examining the role of copper in the pathogenesis of Alzheimer's disease. Remarkably, there is in vitro and animal data to support both copper toxicity and copper deficiency as relevant mechanisms in Alzheimer's disease. These data have prompted preliminary clinical trials of both copper complexing therapy and copper supplementation therapy, which have yielded mixed results. The preclinical and clinical studies are discussed here in an effort to determine how to move forward with rational clinical trials focused on copper modulation.
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Article Evaluation of coenzyme Q as an antioxidant strategy for Alzheimer's disease. 2008
Wadsworth TL, Bishop JA, Pappu AS, Woltjer RL, Quinn JF. · Department of Neurology, Oregon Health & Science University, Portland, OR 97239-3098, USA. · J Alzheimers Dis. · Pubmed #18560133 No free full text.
Abstract: Increasing evidence suggests that Alzheimer's disease (AD) is associated with oxidative damage that is caused in part by mitochondrial dysfunction. Here we investigated the feasibility of modifying Alzheimer pathology with the mitochondrial antioxidant coenzyme Q (CoQ). Exogenous CoQ protected MC65 neuroblastoma cells from amyloid-beta protein precursor C-terminal fragment (APP CTF)-induced neurotoxicity in a concentration dependent manner, with concentrations of 6.25 microM and higher providing near complete protection. Dietary supplementation with CoQ at a dose of 10 g/kg diet to C65/Bl6 mice for one month significantly suppressed brain protein carbonyl levels, which are markers of oxidative damage. Treatment for one month with 2 g lovastatin/kg diet, which interferes with CoQ synthesis, resulted in a significant lowering of brain CoQ10 levels. Mitochondrial energetics (brain ATP levels and mitochondrial membrane potential) were unaffected by either CoQ or lovastatin treatment. Our results suggest that oral CoQ may be a viable antioxidant strategy for neurodegenerative disease. Our data supports a trial of CoQ in an animal model of AD in order to determine whether a clinical trial is warranted.
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