Neuroinflammatory processes

Neuroinflammatory processes encompass the complex innate immune response within the central nervous system (CNS), primarily mediated by glial cells such as microglia and astrocytes (DiSabato et al., 2016). While acute neuroinflammation serves as a protective mechanism to eliminate pathogens and initiate tissue repair, chronic or dysregulated neuroinflammation is a key driver of neuronal damage in conditions like Alzheimer's disease, Parkinson's disease, and Multiple Sclerosis (Glass et al., 2010). This process involves the coordinated release of pro-inflammatory mediators, including cytokines (e.g., TNF-alpha, IL-1 beta), chemokines, and reactive oxygen species, which can compromise the integrity of the blood-brain barrier (Ransohoff, 2016). Because 'neuroinflammatory processes' describe a broad pathological state rather than a single molecular entity, therapeutic intervention typically targets specific receptors, enzymes, or signaling pathways within this cascade (Skaper et al., 2018). Modern drug development aims to shift the CNS environment from a pro-inflammatory (M1-like) state to a pro-resolving or neuroprotective (M2-like) state to mitigate neurodegeneration (Leng & Edison, 2021).

Other names

NeuroinflammationCNS inflammationBrain inflammationNeuroinflammatory response

Modulation of microglial and astrocytic activation states, inhibition of pro-inflammatory cytokine and chemokine signaling, stabilization of the blood-brain barrier, and reduction of oxidative stress within the central nervous system.