Microglia: Scapegoat, Saboteur, or Something Else?
By A. Aguzzi, B. Barres, Mariko L. Bennett. Science, 2013
826 citations recorded by the source corpus.
Microglia are resident immune cells in the brain and spinal cord. These cells provide immune surveillance and are mobilized in response to disparate diseases and injuries. Although microglial activation is often considered neurotoxic, microglia are essential defenders against many neurodegenerative diseases. It also seems increasingly likely that microglial dysfunction can underlie certain neurological diseases without an obvious immune component.
Subfields: Developmental Neuroscience, Neurology
View Paper: https://www.semanticscholar.org/paper/80094db0f95bb81888df983bf42d1aa0958fcfb4
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In Developmental Neuroscience
In Neurology
Citations in the corpus
- Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation (2016, neutral): “Although it has been postulated that excessive microglial activation may promote neurodegeneration (Aguzzi et al., 2013), the exact mechanisms remain unclear.”
- Temporal Tracking of Microglia Activation in Neurodegeneration at Single-Cell Resolution (2017, background): “They clear apoptotic cells and are involved in both the elimination and maintenance of synapses for proper neural circuit wiring (Aguzzi et al., 2013).”
- iPSC-derived human microglia-like cells to study neurological diseases (2017, neutral): “Microglia along with astrocytes, also play a critical role in synaptic pruning (Aguzzi et al., 2013, Paolicelli et al., 2011, Stephan et al., 2012).”
- Role of ROS and RNS Sources in Physiological and Pathological Conditions (2016, background): “This occurs in the normal aging process due to mitochondrial derived ROS production, which promotes inflammation and cytokine production [414].”
- Alzheimer’s Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta (2013, neutral): “Microglial cells regulate Ab levels in the brain by a process of uptake and degradation, which plays a key role in AD pathogenesis (Aguzzi et al., 2013; Prinz et al., 2011).”
- In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer’s disease model (2013, background): “Besides astrocytes, NG2 cells and microglia can also be activated and proliferate rapidly in the injury sites or in diseased brain (Aguzzi et al., 2013; Hines et al., 2009; Kang et al., 2013).”