Novel or Experimental Interventions Targeting Traumatic Brian Injury (TBI)
Classification | Mechanism/Rationale |
---|---|
Cell cycle inhibitors (e.g., flavopiridol) (58, 64) | Reduces neuronal cell death, reduces astroglial scar formation, decreases lesion volume, improves experimental motor and cognitive performance |
Magnesium salts (49, 52, 58) | Blocks calcium entry, potentiates adenosine action, attenuates brain edema, cerebral vasospasms, glutamate excitotoxicity, calcium-mediated events, lipid peroxidation, mitochondrial permeability transition, and apoptosis |
Cyclosporin A (49, 52) | Inhibits opening of the mitochondrial permeability transition pore, attenuates post-traumatic cytoskeletal changes and axonal injury, decreases lesion volume, improves brain oxygen consumption, blocks free radical production, and inhibits traumatic axonal injury |
Substance P (neurokinin 1) receptor inhibitor (52, 58) | Reduces neurogenic inflammation, blood-brain barrier permeability, edema, lesion volume |
Progesterone (32, 49, 52, 58) | Modulates neuronal excitability, reduces membrane lipid peroxidation, and inhibits caspase-3 activation |
Cannabinoids (49, 58) | Reduces glutamate excitotoxicity, free radical production, and inflammatory response |
Cyclic dipeptides (58) | Attenuates apoptotic and necrotic cell death, reduces intracellular calcium, stabilizes mitochondrial membrane potential, and decreases cytochrome c release |