Do amyloid beta-associated factors co-deposit with Abeta in mouse models for Alzheimer's disease?

Abstract

Senile plaques and cerebral amyloid angiopathy in Alzheimer's disease (AD) patients not only consist of the amyloid-beta protein (Abeta), but also contain many different Abeta-associated factors, such as heparan sulfate proteoglycans, apolipoproteins, and complement factors. These factors may all influence Abeta deposition, aggregation, and clearance and therefore seem important in the development of human Abeta deposits. To study AD pathology and test new therapeutic agents, many different mouse models have been created. By transgenic expression of the amyloid-beta protein precursor, frequently in combination with other transgenes, these animals develop Abeta deposits that morphologically resemble their human counterparts. Whether this resemblance also applies to the presence of Abeta-associated factors is largely unclear. In this review, the co-deposition of factors known to associate with human Abeta deposits is summarized for several different AD mouse models.