About this Research Topic
Inflammation in the central nervous system (CNS) injury can produce a variety of acute neurological damage that lead to neuronal cell death. In the CNS, microglia are the resident macrophages, and they are a key player in its immune responses. They respond to extracellular signals and are involved in clearing debris and toxic substances by phagocytosis, thereby retaining normal cellular homeostasis following CNS injury. Consequently, under physiological states, there is continuous, low-level microglial activity in the CNS which is primarily involved in activity-dependent synaptic pruning and repair. In the event of acute CNS insults such as trauma, ischemia, and neurodegeneration, microglia are readily activated by undergoing morphologic transformation from a “ramified” resting state to an active, motile “amoeboid” state. Microglial activation plays a major role in neuronal cell damage by releasing a variety of inflammatory and neurotoxic mediators. Although, the activated microglia exacerbate CNS injury and release a variety of other stressors in the acute stages, they are also essential for brain recovery and repair. For this reason, modulation of microglial phenotype is clearly an important topic of investigation, and represents a huge potential for the development of new therapeutic strategies in acute CNS injury (as well as chronic neurodegenerative diseases). However, the insight of microglial activities is still not completely understood, although there is accumulating knowledge about their role following CNS injury.
In this Research Topic, we aim to describe an overview on the modulation of microglia transition activity phenotype and their role in inflammation following CNS injury, such as stroke, trauma, neurodegenerative disease, and spinal cord/peripheral nerve injury. The articles describing the current knowledge on any aspect regarding microglia activation-induced neuron death or neurogenesis are also welcome. Although this research topic mainly concerns the microglia transition activity regarding neurological aspects, we also welcome all biological topics related to microglial function and interaction with macrophage.
Keywords: CNS injury, Inflammation, Microglia, Neuronal death, Neurorepair
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