In an unbiased elderly population, immunophenotyping of microglia using markers associated with specific microglial functions (Fig. 2) has revealed that in AD, microglia appear to lose motility-associated proteins (e.g. Iba1), a key function in synaptic support [36] and change towards a more phagocytic phenotype (CD68, macrophage scavenging receptor (MSR)-A), partly driven by the APOE genotype [14]. This evidence concerns the gene APOE and Alzheimer disease.