| First Author | Fan LF | Year | 2013 |
| Journal | Neurosci Lett | Volume | 548 |
| Pages | 255-60 | PubMed ID | 23748076 |
| Mgi Jnum | J:201534 | Mgi Id | MGI:5514302 |
| Doi | 10.1016/j.neulet.2013.05.055 | Citation | Fan LF, et al. (2013) Caspr interaction with Amyloid Precursor Protein reduces amyloid-beta generation in vitro. Neurosci Lett 548:255-60 |
| abstractText | Contactin associated protein (Caspr), an adhesion molecule, plays roles in formation of paranodal junctions in myelinated axons, neurite outgrowth, synaptic plasticity in nervous system. Here we have shown a novel function of Caspr in pathogenesis of Alzheimer's disease (AD). Caspr distributes around amyloid plaques in APP/PS1 mice. Levels of Caspr increase in the cerebral cortex of 7-month-old APP/PS1 mice comparing to wild-type littermates. Caspr decreased protein levels of APP in both HEK-293 cells stably transfected with Indiana mutant APP (V717F; HEK-APP) and CHO cells which express endogenous APP, while it did not alter mRNA levels of APP. Furthermore, Caspr co-localizes and interacts with APP. Amyloid-beta (Abeta) 40 and Abeta42 generation were also reduced in HEK-APP cells by Caspr overexpression. |
