| First Author | Janssen L | Year | 2016 |
| Journal | Biochim Biophys Acta | Volume | 1862 |
| Issue | 1 | Pages | 105-12 |
| PubMed ID | 26542217 | Mgi Jnum | J:255465 |
| Mgi Id | MGI:6105265 | Doi | 10.1016/j.bbadis.2015.10.027 |
| Citation | Janssen L, et al. (2016) Late age increase in soluble amyloid-beta levels in the APP23 mouse model despite steady-state levels of amyloid-beta-producing proteins. Biochim Biophys Acta 1862(1):105-12 |
| abstractText | Age is considered the most important risk factor for Alzheimer's disease. Soluble amyloid-beta (Abeta) has been implicated as the primary neurotoxic agent in Alzheimer's disease pathology. The link between aging and Abeta, however, remains unclear. In this study, we aimed to investigate the evolution of soluble Abeta over various age groups in the APP23 amyloidosis mouse model and correlate these changes to alterations in the levels of proteins involved in Abeta production. We found a distinct pattern with an initial buildup of Abeta which could be linked to an increase in amyloid precursor protein (APP). Following this increase, Abeta concentrations remained stable until a surge in Abeta1-42 at 18 months. This rise was followed by an increase in Abeta1-40 and overall Abeta levels. The rise in Abeta at later age did not correlate to changes in the levels of APP, presenilin, and beta-secretase and is suggested to result from a decrease in clearance. The APP23 model could provide an interesting tool for future research regarding aging and Abeta clearance. |
