Unraveling the normal physiologic role of β-amyloid is likely crucial to understanding the pathogenesis of Alzheimer's disease. However, progress on this question is currently limited by the high background of many ELISAs for murine β-amyloid. Here, we examine the background signal of several murine β-amyloid ELISAs, and conclude that the majority of the background is from non-APP derived proteins. Most importantly, we identify ELISAs that eliminate this background signal.