neuroprotection

Neuroprotection is a field devoted to preserving neuronal structure and function after brain or spinal cord injury, stroke, or neurodegenerative disease. The goal is to reduce neuronal death and dysfunction by interrupting secondary injury cascades that follow an initial insult, such as excitotoxicity from excessive glutamate, oxidative stress, inflammation, mitochondrial dysfunction, and disturbances in calcium signaling and energy metabolism.

Key mechanisms and targets include minimizing excitotoxic damage, stabilizing calcium homeostasis, scavenging reactive oxygen species, damping neuroinflammation, and maintaining mitochondrial integrity to prevent cell death pathways such as apoptosis and necroptosis. Neuroprotective strategies may also aim to bolster endogenous repair processes, such as autophagy, and enhance neuronal resilience through neurotrophic signaling.

Approaches span pharmacological and non-pharmacological domains. Pharmacological strategies have included NMDA receptor antagonists (for example, memantine), calcium channel blockers, antioxidants (such as edaravone), anti-inflammatory agents (including certain tetracyclines), and agents that support mitochondrial function or inhibit specific cell-death pathways. Neurotrophic factors and certain modulators of cellular stress responses have been explored as well. Non-pharmacological approaches include therapeutic hypothermia, ischemic or remote ischemic conditioning, exercise, caloric restriction, and sleep optimization, which may complement drug therapies.

Clinical translation has been challenging. While neuroprotective concepts show promise in experimental models, many interventions have had limited or context-specific success in humans, due to timing, dosing, patient heterogeneity, and safety concerns. Ongoing research emphasizes multimodal strategies, biomarkers, and personalized approaches to improve outcomes in acute injuries (such as stroke and traumatic brain injury) and chronic neurodegenerative diseases.