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.
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.
A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.
TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.
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.
A cell-cell contact between microglial SIRPα and CD47 on neighboring cells is a critical module for phase conversion of microglia in the brain white matter and controls demyelination.
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.
Embryonic and definitive macrophages require colony-stimulating factor 1 receptor, whereas non-hematopoietic metaphocytes that resemble macrophages do not, explaining the relative high numbers of putative macrophages in Csf1r-deficient zebrafish.
