Because rapid treatment following suspected traumatic brain injury is linked with survival and recovery, having a biomarker that can be used as a diagnostic has great human health importance. Molecular biomarkers used in human health applications are often applicable to other mammals; specifically for veterinary medicine. However, application for risk management of nonmammalian wildlife has been limited or difficult due to the lack of specific biomarkers for exposure and effect to environmental, chemical, or physical stressors. This study details the unique application of a molecular biomarker for human brain injury in a non-mammalian species for use in wildlife risk management. The routine application of molecular biomarkers in field monitoring and testing has been limited to veterinary health. However, increasing use of risk-surveillance approaches for identification of health issues in livestock are being accepted for both strategic and operational purposes. While disease and vector transmission implications to human health are the drivers for this type of risk management, the animal populations in question are monitored for disease exposure, overall health and productivity. The extension of incorporating molecular markers for contaminant/disease exposure has been documented for assessing wild populations of organisms at all trophic levels. However, the specificity of many of these markers, or biomarkers, remains questionable for AMG-47a wildlife management practices. Aside from biological or chemical exposures, there has been no documented assessment of acute or sub-lethal injury impacts resulting from physical trauma in wildlife. The importance of this study illustrates the success in using a biomarker for mammalian or human head injury to determine head injury in migrating juvenile salmon as a result of hydropower passage management; and represents the first study to examine the efficacy of a human-based molecular biomarker metric for risk management. Unique and differential aII-spectrin breakdown products were first shownto be generated by calpain and caspase proteases incellculture neurotoxic models and in vitro, producing SBDP150/SBDP145 and SBDP150i/SBDP120, respectively. Pike and colleagues were also the firstto observe the same major SBDPsin different affected rat brain regions and in the cerebrospinal fluid compartment following experimental traumatic brain injury. In the current study,Amiselimod hydrochloride spillway force-induced brain injury in salmon brain robustly produces SBDPs parallel to those produced by their mammalian counterparts. When compared with the visible injury observations 48 hours post passage, the trends in passage impact correlate with the presence of SBDP120. In particular, the abundance of SBDP120 shows increasing expression with increasing visible injury. Predicted amino acid sequence homology for the SBDP120 cleavage site, and binding of the specific SBDP120 antibody provide strong evidence for conservation of functional homology. Based on the known mammalian expression pattern, the increase in expression is hypothesized to be evidence of apoptotic breakdown of intact aII-spectrin, a likely event that would occur following physical traumato brain tissues. The lack of complete homology of mammalian SBDPs in salmon brain tissues may be related more to the evidence of genome duplication in the salmonids and the loss of function due to redundancy, or adaptation for different functions.Without a complete aII-spectrin sequence in salmon, these remain assumptions. In addition, activation of Akt signalling stimulates and importantly increases ischemia induced mobilization of endothelial progenitor cells.