| First Author | Rupp NJ | Year | 2011 |
| Journal | Neurobiol Aging | Volume | 32 |
| Issue | 12 | Pages | 2324.e1-6 |
| PubMed ID | 20970889 | Mgi Jnum | J:188225 |
| Mgi Id | MGI:5439712 | Doi | 10.1016/j.neurobiolaging.2010.08.014 |
| Citation | Rupp NJ, et al. (2011) Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic mice. Neurobiol Aging 32(12):2324.e1-6 |
| abstractText | APPPS1 transgenic mice develop amyloid-beta 42 (Abeta42)-driven early-onset cerebral beta-amyloidosis. Stereological analysis of neocortical neuron number in groups of 2-, 10-, and 17-month-old APPPS1 mice did not reveal any changes compared with wild-type control animals despite massive amyloid-beta (Abeta) load and disrupted cytoarchitecture. However, in subregions with high neuron density such as the granule cell layer of the dentate gyrus, modest but significant neuron loss was found, reminiscent of findings in previously published mouse models with late onset cerebral beta-amyloidosis and predominant amyloid-beta 40 (Abeta40) expression. |
