Gene knockout of amyloid precursor protein and amyloid precursor‐like protein‐2 increases cellular copper levels in primary mouse cortical neurons and embryonic fibroblasts

• DOI: 10.1111/j.1471-4159.2004.02731.x
• Publication Date: 2004-09-24T12:55:31Z
• Authors: Shayne A. Bellingham; Giuseppe D. Cicco...; B. Elise Needham; Lisa R. Fodero; Anthony R. White; Colin L. Masters; Roberto Cappai; James Camakaris
• Keywords: BACE1-AS; P3 peptide; Amyloid (mycology)

Abstract Alzheimer's disease is characterised by the accumulation of amyloid‐β peptide, which cleaved from copper‐binding precursor protein. Recent in vivo and vitro studies have illustrated importance copper neuropathogenesis suggested a role for protein homeostasis. Amyloid‐β member multigene family, including amyloid precursor‐like proteins‐1 ‐2. The domain similar among family members, suggesting an overall conservation its function or activity. Here, we demonstrate that double knockout protein‐2 expression results significant increases mouse primary cortical neurons embryonic fibroblasts. In contrast, over‐expression transgenic mice significantly reduced levels neurons. These findings provide cellular neuronal evidence homeostasis support existing hypothesis are proteins with functionally interchangeable roles