These results were interpreted to suggest that in these animal models of AD, (1) early complement activation (as indicated by C1q deposition) in response to fibrillar Aβ deposition might be responsible for the chemotactic attraction of activated glial cells, and (2) the activated microglia, while unable to clear fibrillar Aβ, may have contributed to the loss of neuronal integrity indicated by reduced MAP-2 and synaptophysin staining in the APP mice. This evidence concerns the gene APP and Alzheimer disease.