Neuroinflammatory signaling pathway

Neuroinflammatory signaling pathways encompass the collection of molecular and cellular signaling mechanisms that drive neuroinflammation, primarily in the central nervous system (CNS). Key drivers include cytokines, chemokines, kinases, and transcription factors such as NF-κB, MAPK, PI3K-Akt, NLRP3 inflammasome, and Nrf2 pathways. These diverse pathways regulate glial cell activation, immune cell recruitment, cytokine production, oxidative stress responses, and neuronal survival or death. Dysregulation is central to the pathogenesis of several neurodegenerative and inflammatory CNS disorders, but due to the complexity and broadness, “neuroinflammatory signaling pathways” is not a suitable standalone drug target, rather it guides the identification and therapeutic modulation of its specific molecular components (e.g., CCL2-CCR2, NF-κB, or Nrf2)[2][3][4][5][6][7][8]. Summary judgment: "Neuroinflammatory signaling pathways" is an umbrella term for multiple mechanisms involved in CNS inflammation and is not a valid molecular target per drug discovery, structure, or nomenclature standards. Individual pathways or molecules within this set (e.g., NF-κB, CCR2, Nrf2) are appropriate targets.

Other names

Neuroinflammation pathwaysNeuroinflammatory pathwaysCentral nervous system inflammatory signaling