Editorial on the Research Topic
Neuroendocrine Disorders After Traumatic Brain Injury: Past, Present and Future
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Traumatic brain injury (TBI) has reached epidemic proportions worldwide with an increasing number of individuals being exposed as a sequela of contact sports, motor vehicle accidents or warfare. Long recognized as a potential cause for pituitary hormone deficiency (PHD), TBI is also increasingly emerging as a research priority given that, in this setting, the prevalence of PHD, the pathophysiologic mechanisms and the response to hormone replacement have not been well-established.
Several important papers published in this issue of Frontiers in Endocrinology bring new light to this area. Zhou et al. provide intriguing gene expression data for brain glucose metabolism alterations in a mouse model post-TBI that correspond with previous reports of changes in brain glucose utilization in patients post-TBI. The fact that these alterations were responsive to Telmisartan (a well-known neuroprotective agent and FDA-approved drug that was originally used to treat hypertension) opens potential therapeutic avenues that could be tested further in other animal models and, if confirmed, subsequently in human studies.