engleski

Changes in the hippocampal amyloid-beta precursor protein expression following single moderate and repetitive traumatic brain injury

Introduction/Objectives: Traumatic brain injury (TBI) is a major cause of death and disability among young individuals. Mild TBI occurs with far greater frequency than moderate or severe TBI, usually as a consequence of collisions in contact sports, domestic violence, or war events. Moderate and severe TBI is generally a result of falls or car accidents. It is well known that severe TBI presents one of the risk factors for the development of neurodegenerative disorders such as Alzheimer's disease (AD), while the role of mild and moderate TBI in the development of AD is still undetermined. Amyloid-beta precursor protein (APP) is a ubiquitous membrane protein involved in synapse formation, neural plasticity, iron export, and antimicrobial activity. Also, the processing of APP can lead to the formation of neurotoxic amyloid-beta peptide. The aim of this study was to investigate the hippocampal expression of APP in the male adult C57BL/6 mice, 14 days following single moderate or repetitive mild brain trauma. Participants, Materials/Methods: Lateral fluid percussion injury (LFPI) was used as a model of a single moderate TBI. Trauma was induced over the left parietal cortex. Another cohort of mice received mild repetitive brain traumas induced by the weight drop method, twice a day, during 5 consecutive days. Traumatized animals were sacrificed 14 days after LFPI or the last mild head impact, and their hippocampi were prepared for the western blot analyses. Sham-injured animals from both TBI models were used as the control groups. Results: In the hippocampi of animals subjected to repetitive mild brain trauma, we detected a significant increase in the expression of the mature form of APP, while the total and immature APP levels remained unchanged. Single moderate TBI did not cause changes in mature, immature nor total APP levels at 14 days post-LFPI. Conclusions: Our preliminary results suggest that hippocampal changes in the APP mature form, at 14 days after trauma, are only evident after mild repetitive but not single moderate brain trauma. This indicates that there are some variations in the pathophysiology of posttraumatic neurodegenerative disorders which depend on the type of TBI suffered by the individuals. This work was supported by the University of Rijeka, Croatia, project uniri-biomed-18-199 to K.P. and Croatian Science Foundation, project IP-2016-06-4602 to G.Ž.

Amyloid-beta precursor protein, Hippocampus, Traumatic brain injury

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