Neuroinflammatory and oxidative stress pathways

Neuroinflammatory and oxidative stress pathways represent a complex network of biological processes where immune activation and the production of reactive oxygen species (ROS) mutually reinforce each other, leading to neuronal damage (PubMed: PMC6139815). In the central nervous system, chronic activation of microglia and astrocytes triggers the release of pro-inflammatory cytokines (e.g., TNF-alpha, IL-1beta) and oxidative markers, which are hallmark features of neurodegenerative diseases like Alzheimer's and Parkinson's (Nature: s41583-018-0012-4). Therapeutic strategies often focus on dual-action agents that can simultaneously upregulate antioxidant defenses, such as the Nrf2 pathway, while inhibiting pro-inflammatory signaling via NF-kB (Journal of Neuroinflammation: 10.1186/s12974-020-01913-9). While these pathways are critical for disease progression, they do not represent a single molecular target but rather a cascade of interacting proteins and signaling molecules (Frontiers in Pharmacology: 10.3389/fphar.2020.00694). Consequently, drug development in this area often targets specific nodes within these pathways, such as the NLRP3 inflammasome or NADPH oxidase, to achieve neuroprotection (PubMed: PMC7284351).

Other names

Neuroinflammation-oxidative stress axisRedox-inflammatory signaling cascadeNeuroinflammatory-oxidative stress crosstalkOxidative stress and neuroinflammation

Modulation of redox-sensitive transcription factors (e.g., Nrf2, NF-kB) and inhibition of pro-inflammatory enzyme activity (e.g., COX-2, iNOS) to mitigate oxidative damage and neuroinflammation.