| First Author | Nishida Y | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 350 |
| Issue | 3 | Pages | 530-6 |
| PubMed ID | 17026966 | Mgi Jnum | J:114504 |
| Mgi Id | MGI:3689247 | Doi | 10.1016/j.bbrc.2006.09.083 |
| Citation | Nishida Y, et al. (2006) Deletion of vitamin E enhances phenotype of Alzheimer disease model mouse. Biochem Biophys Res Commun 350(3):530-6 |
| abstractText | 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. |
