Research in the past decade has identified new molecular risk factors that implicate these brain immune cells in Alzheimer’s disease. Conversely, people who are APOE2 carriers are at lower risk for developing Alzheimer’s and are much less likely to develop amyloid pathology. Again, amyloid mouse models with the R47H variant developed more neuritic plaque tau pathology near amyloid plaques when injected with tau seeds. This finding suggested that reducing microglial activity resulted in less damage and brain atrophy from tau pathology. In tau mouse models, mice that received the drug exhibited dramatically reduced tau pathology and neurodegeneration, indicating that microglia are required for tau-dependent neurodegeneration.