Oxidative stress pathways in neurons

The term "oxidative stress pathways in neurons" does not refer to a single molecule, receptor, or traditional drug target but rather to a complex network of molecular processes involving the balance between production of reactive oxygen species (ROS) and cellular antioxidant responses in neuronal cells[2][1][3][5]. Key molecular elements include transcription factors such as NRF2 (which regulates antioxidant gene expression via the ARE pathway) and NF-κB (which mediates inflammation and apoptosis in response to ROS/RNS)[2][4]. These pathways are implicated in neuron vulnerability, mitochondrial dysfunction, calcium dysregulation, chronic inflammation, and glutamate excitotoxicity[1][5]. Oxidative stress in neurons is a central mechanism contributing to neurodegenerative diseases such as Alzheimer's and Parkinson's disease, stroke, and other CNS disorders[2][5]. Current therapeutic approaches focus on antioxidants and pathway modulators; however, the term as presented does not represent a singular, druggable molecular entity, but rather an aggregate of interrelated cellular and molecular responses to redox imbalance[2][3][4].

Other names

neuronal oxidative stress pathwaysneuronal ROS/RNS pathwaysneuronal redox pathways

ROS scavenging, NRF2-ARE pathway activation, NF-κB pathway inhibition, MAPK pathway inhibition