| First Author | Mahler J | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 7 | Pages | 2241-2247 |
| PubMed ID | 25911278 | Mgi Jnum | J:224496 |
| Mgi Id | MGI:5662354 | Doi | 10.1016/j.neurobiolaging.2015.03.011 |
| Citation | Mahler J, et al. (2015) Endogenous murine Abeta increases amyloid deposition in APP23 but not in APPPS1 transgenic mice. Neurobiol Aging 36(7):2241-2247 |
| abstractText | Endogenous murine amyloid-beta peptide (Abeta) is expressed in most Abeta precursor protein (APP) transgenic mouse models of Alzheimer's disease but its contribution to beta-amyloidosis remains unclear. We demonstrate approximately 35% increased cerebral Abeta load in APP23 transgenic mice compared with age-matched APP23 mice on an App-null background. No such difference was found for the much faster Abeta-depositing APPPS1 transgenic mouse model between animals with or without the murine App gene. Nevertheless, both APP23 and APPPS1 mice codeposited murine Abeta, and immunoelectron microscopy revealed a tight association of murine Abeta with human Abeta fibrils. Deposition of murine Abeta was considerably less efficient compared with the deposition of human Abeta indicating a lower amyloidogenic potential of murine Abeta in vivo. The amyloid dyes Pittsburgh Compound-B and pentamer formyl thiophene acetic acid did not differentiate between amyloid deposits consisting of human Abeta and deposits of mixed human-murine Abeta. Our data demonstrate a differential effect of murine Abeta on human Abeta deposition in different APP transgenic mice. The mechanistically complex interaction of human and mouse Abeta may affect pathogenesis of the models and should be considered when models are used for translational preclinical studies. |
