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Neuroinflammation-related markers and pathways refer to the collective set of molecular signals and cellular processes that mediate the immune response within the central nervous system (CNS). This broad category involves the activation of resident glial cells, primarily microglia and astrocytes, and the subsequent production of inflammatory mediators such as cytokines (e.g., Tumor necrosis factor-alpha, Interleukin-1 beta), chemokines, and reactive oxygen species [1][2]. While acute neuroinflammation serves a protective role in response to injury or infection, chronic activation of these pathways is a hallmark of neurodegenerative conditions, including Alzheimer's disease, Parkinson's disease, and Multiple sclerosis [3][4]. Therapeutic interventions targeting these pathways aim to suppress neurotoxic inflammatory cascades or promote pro-resolving phenotypes in immune cells to prevent neuronal loss [5]. Key molecular targets within this framework include the NLRP3 inflammasome, various Toll-like receptors, and specific cytokine signaling axes [6].
Inhibition of pro-inflammatory cytokine signaling, modulation of microglial and astrocytic activation states, blockade of leukocyte trafficking into the central nervous system, and inhibition of the NLRP3 inflammasome assembly and activation.
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