Microglia and neuroinflammatory signaling

Microglia are the primary resident immune cells of the central nervous system, responsible for immune surveillance, synaptic pruning, and maintaining tissue homeostasis (Colonna, M., & Butovsky, O., 2017, 'Microglia Function in the Central Nervous System During Health and Neurodegeneration', Annual Review of Immunology). Neuroinflammatory signaling involves the activation of these cells in response to pathological stimuli, such as amyloid-beta plaques or alpha-synuclein aggregates, leading to the production of cytokines, chemokines, and reactive oxygen species (Glass, C. K., et al., 2010, 'Mechanisms underlying inflammation in neurodegeneration', Cell). While transient signaling is essential for repair, chronic neuroinflammation is a key driver of neurodegeneration in conditions like Alzheimer's disease, Parkinson's disease, and Amyotrophic Lateral Sclerosis (Heneka, M. T., et al., 2015, 'Neuroinflammation in Alzheimer's disease', The Lancet Neurology). Pharmacological intervention focuses on modulating specific microglial receptors and pathways, such as the NLRP3 inflammasome, TREM2, and CSF1R, to reduce neurotoxicity and promote neuroprotection (Subhramanyam, C. S., et al., 2019, 'Microglia-mediated neuroinflammation in neurodegenerative diseases', Seminars in Cell & Developmental Biology).

Other names

Microglial activationNeuroinflammationCNS inflammatory signalingMicroglial-mediated neurodegeneration

Inhibition of pro-inflammatory cytokine production, modulation of microglial phenotype (M1 to M2 transition), and blockade of specific receptors like CSF1R or the NLRP3 inflammasome.