engleski

THE EFFECTS OF REPETITIVE MILD TRAUMATIC BRAIN INJURY ON SOME PROTEINOPATHY SUSCEPTIBLE PROTEINS IN THE MOUSE FRONTAL CORTEX

Introduction: Traumatic brain injury (TBI) is an important healthcare problem leading to lifelong repercussions that burden society. Primary brain injury is irreversible, but secondary TBI includes many pathophysiological processes, including the development of proteinopathies that contribute to cognitive impairment. This study aimed to investigate the expression of amyloid-beta precursor protein (APP), phosphorylated Tau protein (pTau) and TAR-DNA binding protein 43 (TDP-43) in the frontal cortex of C57BL/6 mice 14 days after mild repetitive traumas. Selected proteins are susceptible to pathological misfolding and are proven to contribute to the clinicopathological spectrum of dementias developing after TBI. Materials/Methods: Repetitive mild brain traumas were applied by the weight drop method, twice per day, 5 days in a row. Injured animals were sacrificed 14 days after the last brain trauma and their frontal cortices were prepared for western blot or immunohistological analyses. Control group of animals were sacrificed one day after the sham injury procedure. Results: At 14 days post-injury, a significant increase in the cortical expression levels of total and mature APP was detected, while pTau positive cells were not found. A significant increase in the TDP-43 levels was detected only in the nucleus, but cytoplasmic mislocalization and phosphorylation were not found after mild repetitive TBI. Conclusions: Our preliminary results showed that repetitive brain traumas lead to changes in APP levels at 14 days, without the formation of pathological pTau and TDP-43 species. 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 GŽ.

Amyloid-beta precursor protein, TAU protein, TDP-43, Cortex, Traumatic brain injury

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