Neuroinflammation, which refers to the inflammatory response occurring in various Central Nervous System (CNS) disorders, is a relatively recent concept. It involves two main types of cells: astrocytes, which play a significant role in the process, and brain myeloid cells (BMC), crucial players in neuroinflammation.Studies examining the entire genome (GWAS) have pinpointed over 30 genetic loci associated with Alzheimer's disease (AD), many of which relate to innate immunity and the function of microglia, notably the apolipoprotein E (APOE) gene. APOE4 is particularly significant, being the strongest genetic risk factor for late-onset AD, with one copy increasing the risk by 3 to 4 times, and two copies by 8 to 10 times. While astrocytes primarily produce APOE in the brain, microglia and neurons also synthesize it during neurodegeneration. APOE expression is heightened in disease-associated microglia (DAM), suggesting its involvement in disease through its immunomodulatory function.We have developed cerebral organoid models containing human microglia and astroglia derived from induced pluripotent stem cells (iPSCs) with either APOE ε3/ε3 or ε4/ε4 genotype for AD dementia and from individuals with normal cognition with similar age . Our objective is to investigate how the differential expression of APOE proteins in microglia and astroglia within brain organoids, as well as the presence of different APOE isoforms, influence the process of neuroinflammation.In this abstract, we aim to present and discuss our findings with fellow experts in the field.