Glutamatergic and oxidative stress-related pathways

Glutamatergic and oxidative stress-related pathways represent a broad physiological and pathological framework rather than a single molecular target (Lewerenz & Maher, 2015). These pathways involve the regulation of glutamate, the primary excitatory neurotransmitter in the brain, and the cellular mechanisms that manage reactive oxygen species (ROS). In many neurological conditions, excessive glutamate release leads to overactivation of receptors like the N-methyl-D-aspartate (NMDA) receptor (Coyle & Puttfarcken, 1993). This overactivation causes a massive influx of calcium that triggers mitochondrial dysfunction and the subsequent generation of free radicals. This interplay is a hallmark of neurodegeneration, where excitotoxicity and oxidative stress form a self-perpetuating cycle of cell death. Therapeutic strategies targeting these pathways often involve NMDA receptor antagonists or antioxidant agents to mitigate neuronal damage. Drugs such as memantine and riluzole are commonly used to modulate these systems in diseases like Alzheimer's and ALS (PubChem). However, because this term describes a complex network of interactions across multiple proteins and metabolic processes, it is not classified as a discrete molecular drug target.

Other names

Glutamate-mediated excitotoxicity and oxidative stressGlutamatergic signaling and redox homeostasisExcitotoxicity-oxidative stress axis

Modulation of ionotropic glutamate receptors and enhancement of antioxidant defense mechanisms to prevent excitotoxic neuronal death (Lewerenz & Maher, 2015).