Dale B. Bosco

TL;DR: It is suggested that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia and the possible mechanisms controlling the post-ischemic activity of microglia.

TL;DR: It is demonstrated that microglia in awake mice have a relatively reduced process area and surveillance territory and that reduced neuronal activity under general anesthesia increases microglial process velocity, extension and territory surveillance and reduced norepinephrine signaling is necessary for these increases.

TL;DR: The results demonstrate that microglial process dynamics are directly influenced by neural activities through norepinephrine signaling in awake animals and indicate the importance of awake imaging for studying microglia-neuron interactions.

TL;DR: It is indicated that microglia merit consideration as a potential target for NMO therapeutic intervention by continuously infusing IgG (NMO patient serum-derived or AQP4-specific mouse monoclonal), without exogenous complement, into the spinal subarachnoid space and by in vivo spinal cord imaging revealed a striking physical interaction between microglial C3a receptor signaling and astrocytes.

TL;DR: TLR4-dependent autophagy regulates microglial polarization and induces ischemic white matter damage via STAT1/6 pathway, and TLR4 deficiency could mimic the phenomenon in microglia functional transformation, and exhibit a protective activity in chronic cerebral hypoperfusion.