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Cell Death Dis. 2010 Oct 28;1:e91. doi: 10.1038/cddis.2010.73.

Dietary zinc supplementation of 3xTg-AD mice increases BDNF levels and prevents cognitive deficits as well as mitochondrial dysfunction.

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Molecular Neurology Unit-Center of Excellence on Aging, University 'G. d'Annunzio', Chieti-Pescara, Italy.


The overall effect of brain zinc (Zn(2+)) in the progression and development of Alzheimer's disease (AD) is still not completely understood. Although an excess of Zn(2+) can exacerbate the pathological features of AD, a deficit of Zn(2+) intake has also been shown to increase the volume of amyloid plaques in AD transgenic mice. In this study, we investigated the effect of dietary Zn(2+) supplementation (30 p.p.m.) in a transgenic mouse model of AD, the 3xTg-AD, that expresses both β amyloid (Aβ)- and tau-dependent pathology. We found that Zn(2+) supplementation greatly delays hippocampal-dependent memory deficits and strongly reduces both Aβ and tau pathology in the hippocampus. We also evaluated signs of mitochondrial dysfunction and found that Zn(2+) supplementation prevents the age-dependent respiratory deficits we observed in untreated 3xTg-AD mice. Finally, we found that Zn(2+) supplementation greatly increases the levels of brain-derived neurotrophic factor (BDNF) of treated 3xTg-AD mice. In summary, our data support the idea that controlling the brain Zn(2+) homeostasis may be beneficial in the treatment of AD.

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