Richard L Veech and William Curtis
The etiology of traumatic brain injury involves opening of the mitochondrial permeability transition pore resulting in cessation of mitochondrial ATP synthesis by the electron transport system with conversion of the energy of the electron transport system from ATP synthesis to heat production causing an increase in brain temperature. Treatment of TBI can be directed to closing of the mitochondrial permeability transition pore by administration of cyclosporine, which binds cyclophilin, a specific protein component of the pore, or by provision of ketone bodies, whose metabolism increases the energy of ATP hydrolysis with closing of the mitochondrial pore.
