Previously, it was assumed that microglial phagocytosis constrains plaque development in Alzheimer’s disease. However, new findings in mouse models of Alzheimer’s disease suggest that preventing phagocytosis leads to a reduction in the number of plaques in the brain. Greg Lemke, PhD, Salk Institute for Biological Studies, San Diego, CA, speaks on the crucial role of TAM receptors in this process. Microglial TAM receptors linked to Alzheimer’s disease, Axl and Mer, were removed in mouse models, to observe the effect of TAM receptor deficiency on the course of disease. In the absence of TAM receptors, microglia were unable to detect and phagocytose plaques in the brain. The TAM deficient mice showed a ten-fold reduction in phagocytosis and 50% reduction in the number of plaques in the brain. Dr Lemke suggests the dense-core plaques of Alzheimer’s disease are constructed by microglial phagocytosis, as looser plaques are condensed and aggregated. This interview took place at the AD/PD™ 2022 Conference in Barcelona, Spain.
