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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse.

Increased oxidative damage is a prominent and early feature in Alzheimer disease (AD). However, whether it is a primary cause or merely a downstream consequence in AD pathology is still unknown. We previously generated alpha-tocopherol transfer protein knockout (Ttpa(-/-)) mice, in which lipid peroxidation in the brain was significantly increased by complete depletion of alpha-tocopherol (alpha-Toc). Here we crossed AD transgenic (APPsw) model mice (Tg2576) with Ttpa(-/-) mice. The resulting double-mutant (Ttpa(-/-)APPsw) mice showed earlier and more severe cognitive dysfunction in the Morris water maze, novel-object recognition, and contextual fear conditioning tests. They also showed increased amyloid beta-peptide ( Abeta) deposits in the brain by immunohistochemical analysis, which was ameliorated with alpha-Toc supplementation. In this report we provide clear evidence indicating that chronic lipid peroxidation due to alpha-Toc depletion enhances AD phenotype in a mouse model.[1]

References

  1. Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse. Nishida, Y., Yokota, T., Takahashi, T., Uchihara, T., Jishage, K., Mizusawa, H. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
 
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