Since, in vivo, beta-amyloid plaques are quite complex, consisting of not only beta-amyloid itself but many other proteins, dystrophic neurites, and reactive astrocytes, we next performed in vitro migration assays to determine if TREM2 knockout cells exhibit impaired migration toward beta-amyloid alone or whether additional signals derived from AD neurons might further influence the association between microglia and plaque pathology. This evidence concerns the gene TREM2 and Alzheimer disease.