Commentary and Update on Ã¢ÂÂThe Mitochondrial Permeability Transition Pore Provides a Key to the Diagnosis and Treatment of Traumatic Brain InjuryÃ¢ÂÂRichard L Veech* and William Curtis
Laboratory of Metabolic Control, NIAAA, NIH, Fishers Lane, Bethesda, MD, USA
- *Corresponding Author:
- Richard L Veech
Laboratory of Metabolic Control, NIAAA
NIH, 5625 Fishers Lane, Rm 2S 28, Bethesda
MD 20862, USA
Tel: 301 580 4528
E-mail: [email protected]
Received date: December 12, 2016; Accepted date: January 31, 2017; Published date: February 07, 2017
Citation: Veech RL, Curtis W (2017) Commentary and Update on “The Mitochondrial Permeability Transition Pore Provides a Key to the Diagnosis and Treatment of Traumatic Brain Injury”. J Neurol Neurophysiol 8:412. doi:10.4172/2155-9562.1000412
Copyright: © 2017 Veech RL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.