Thiamin rescues cellular respiration after traumatic brain injury. Might this be a promising therapeutic approach?
The team around biophysicist Andrey Kozlov gives answers to this questions in a new publication which is about to be published in BBA – Bioenergetics.
Their interest is based on the fact that traumatic brain injuries are the most common reason for permanent work disability among young adults and mean a great loss of their quality of life. Physical and mental deficits are not only caused by the traumatic injury of brain tissue but also in course of the subsequent inflammation of neurons and disturbances of the cerebral flood flow. Both effects cause more and more neurons to die and brain tissue to deteriorate.
It is know that traumatic brain injury causes malfunction of the mitochondria (the so-called cellular powerhouses) in affected neurons. This is of great concern, as mitochondria are essential for the production of energy in the form of ATP (adenosine triphosphate). The hereby involved biochemical processes are summarized under the term “cellular respiration”.
Under experimental conditions, Kozlov’s team was able to characterize the damage on the mitochondria as a result of traumatic brain injury more accurately. They demonstrated that the activity of a certain enzyme complex (the 2-oxoglutarate dehydrogenase complex, OGDHC) is impaired. This leads to a decrease in cellular respiration and ATP production, crucial factors for cell survival.
The team was able to show that the administration of thiamin – a precursor of a proenzyme necessary for OGDHC function – diminishes the mitochondrial damage and restarts cellular respiration.
Further studies on thiamin now aim to verify the clinical relevance of thiamin application and define the substance’s therapeutic potential.