In addition, higher levels of expression have been observed in subsets of microglia thought to mediate neuroinflammation, such as disease-associated microglia in 5xFAD mice, a widely used mouse model of Alzheimer’s disease and Ccl3/Ccl4-positive microglia in aged and white matter-injured brain, as well as at embryonic and postnatal ages of development (Fig. 3c, [53, 54]). This evidence concerns the gene CCL3 and early-onset autosomal dominant Alzheimer disease.