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.
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.
The microenvironment of brain tumors can be modulated by in vivo conditions that change the brain levels of BDNF and IL-15, with effects on innate immune cell activation.
Pre-neoplastic cells in the brain release SDF1, which mediates an immediate infiltration of macrophages that differentiate into microglia-like cells and promote proliferation of pre-neoplastic cells.
Structural, biophysical, and functional analyses reveal that mutations in TREM2 trigger either misfolding or reduced binding to cell-surface glycosaminoglycans, which segregate with neurodegenerative disease link and highlight a functional surface linked to the pathogenesis of Alzheimer's disease.
Determining that microbiota-deficient mice have increased visceral pain, which can be reversed by restoring microbiota, may lead to novel microbial-based strategies for disorders associated with visceral pain.
High variability in neuropathology burden and interactions between dementia diagnosis and RNA quality present underappreciated complications when studying dementia in an aged population.
