Research from the Gomez-Nicola lab has provided key findings related to the understanding and targeting of neuroinflammation in Dementia. In recent years, the lab has also explored microglial turnover and development, uncovering significant changes in the dynamics of the microglial population from early development to ageing, and disease. Our findings suggest that disease-associated microglial phenotypes are instructed from early development, and hint at both genetic and environmental determinants underpinning this. Now, the lab has set a direction pivoting to the study of human microglia in health and disease. Our findings, and those in the field, justify a strong need to understand human microglia, based on the demonstrated disparity with rodent microglia in the context of diseases like Alzheimer’s. We have a range of techniques, and samples, enabling complex and deep phenotyping and mechanistic studies in human microglia, including Imaging Mass Cytometry (IMC), iPSC-derived microglia and their integration in brain organoids. We are working on other models to enable the study of human microglia in context, which are amenable to higher throughput screening of mechanisms and drugs. Combining our expertise in microglia from development to neurodegeneration, we want to focus on understanding the linkage of cellular trajectories during a healthy lifespan with the onset of cell phenotypes associated to disease initiation and progression. Life-long exposures to environmental stimuli can condition microglia to undergo disease-associated changes, and now we (the field) are in a unique position to uncover these links.