These data indicate that partial CX3CR1 deficiency in heterozygous PS1-APP-CX3CR+/− is associated with a significant reduction in Aβ deposits and load and in the levels of Aβ (1-42) and (1-40) compared to PS1-APP mice and that complete deletion of CX3CR1 is not necessary to confer beneficial effects on AD-like pathology in these mice. This evidence concerns the gene APP and Alzheimer disease.