Purines: forgotten mediators in traumatic brain injury

EK Jackson, D Boison… - Journal of …, 2016 - Wiley Online Library
EK Jackson, D Boison, MA Schwarzschild, PM Kochanek
Journal of neurochemistry, 2016Wiley Online Library
Recently, the topic of traumatic brain injury has gained attention in both the scientific
community and lay press. Similarly, there have been exciting developments on multiple
fronts in the area of neurochemistry specifically related to purine biology that are relevant to
both neuroprotection and neurodegeneration. At the 2105 meeting of the National
Neurotrauma Society, a session sponsored by the International Society for Neurochemistry
featured three experts in the field of purine biology who discussed new developments that …
Abstract
Recently, the topic of traumatic brain injury has gained attention in both the scientific community and lay press. Similarly, there have been exciting developments on multiple fronts in the area of neurochemistry specifically related to purine biology that are relevant to both neuroprotection and neurodegeneration. At the 2105 meeting of the National Neurotrauma Society, a session sponsored by the International Society for Neurochemistry featured three experts in the field of purine biology who discussed new developments that are germane to both the pathomechanisms of secondary injury and development of therapies for traumatic brain injury. This included presentations by Drs. Edwin Jackson on the novel 2′,3′‐cAMP pathway in neuroprotection, Detlev Boison on adenosine in post‐traumatic seizures and epilepsy, and Michael Schwarzschild on the potential of urate to treat central nervous system injury. This mini review summarizes the important findings in these three areas and outlines future directions for the development of new purine‐related therapies for traumatic brain injury and other forms of central nervous system injury.
In this review, novel therapies based on three emerging areas of adenosine‐related pathobiology in traumatic brain injury (TBI) were proposed, namely, therapies targeting 1) the 2′,3′‐cyclic adenosine monophosphate (cAMP) pathway, 2) adenosine deficiency after TBI, and 3) augmentation of urate after TBI.
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