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.
P2ry12-CreER robustly and specifically labels microglia in fate-mapping and ribosomal profiling experiments, revealing new markers for myeloid subpopulations in the central nervous system.
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.
Adult-born neurons in the olfactory bulb that develop in the absence of microglia have a higher density of small spines but weaker excitatory inputs and reduced responses to sensory stimuli.
In mouse models of Rett Syndrome, global loss of the Mecp2 gene induces microglia to engulf excess synapses, while microglia-specific loss or gain of Mecp2 has little impact on disease.
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.
The BMAL1-REV-ERB axis controls expression of complement C4b expression and microglial synaptic phagoctyosis, providing a link between cellular circadian clock function and synaptic regulation.
