Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.
APPPS1 microglia express disease-associated proteomic signatures of Alzheimer's disease earlier, compared to the APP-KI, and these differences correlate with the levels of fibrillar Aβ and impaired microglial phagocytic function.
In an empty microglial niche, repopulating microglia arise from subventricular zone and white matter-associated areas without contributions from the bone marrow to fill the mouse brain via a spreading wave.
During adult neurogenesis in the olfactory bulb, microglia regulate the elimination (pruning), formation, and maintenance of synapses on newborn neurons, contributing to the functional integrity of the olfactory bulb circuitry.
Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.