| First Author | Cheng H | Year | 2010 |
| Journal | Neurobiol Aging | Volume | 31 |
| Issue | 7 | Pages | 1188-96 |
| PubMed ID | 18762354 | Mgi Jnum | J:161991 |
| Mgi Id | MGI:4462135 | Doi | 10.1016/j.neurobiolaging.2008.07.020 |
| Citation | Cheng H, et al. (2010) Apolipoprotein E mediates sulfatide depletion in animal models of Alzheimer's disease. Neurobiol Aging 31(7):1188-96 |
| abstractText | Herein, we tested a recently proposed working model of apolipoprotein E (apoE)-mediated sulfatide metabolism/trafficking/homeostasis with two well-characterized amyloid precursor protein (APP) transgenic (Tg) animal models of Alzheimer's disease (AD) (i.e., APP(V717F) and APPsw) on a wild-type murine apoE background or after being bred onto an Apoe(-/-) background. As anticipated, lipidomics analysis demonstrated that the sulfatide levels in brain tissues were reduced beginning at approximately 6 months of age in APP(V717F) Tg, Apoe(+/+) mice and at 9 months of age in APPsw Tg, Apoe(+/+) mice relative to their respective non-APP Tg littermates. This reduction increased in both APP Tg mice as they aged. In contrast, sulfatide depletion did not occur in APP Tg, Apoe(-/-) animals relative to the Apoe(-/-) littermates. The lack of sulfatide depletion in APP Tg, Apoe(-/-) mice strongly supports the role of apoE in the deficient sulfatide content in APP Tg, Apoe(+/+) mice. Collectively, through different animal models of AD, this study provides evidence for an identified biochemical mechanism that may be responsible for the sulfatide depletion at the earliest stages of AD. |
