Additionally, our results align with previous studies using preclinical models of neurological injuries, such as ischemic injury of the corpus callosum, Alzheimer’s disease, and multiple sclerosis (MS) [16,27,33,39], which have shown that 3K3A-APC treatment can effectively inhibit microglial migration and activation.Furthermore, the increase in inflammatory cells in the CNV area can be attributed to the infiltration of circulating CD11b+ monocytes positive for various proangiogenic factors and inflammatory cytokines [38]. This evidence concerns the gene APC and early-onset autosomal dominant Alzheimer disease.