Search

Introduction: Traumatic brain injury (TBI) represents a burden to healthcare due to limited management options and long-term consequences. The latter are underrepresented and contribute to naming TBI a “silent epidemic“. Neuroinflammation appears to have a significant role in the development of secondary brain injury, involving processes affecting both resolution and persistence of inflammation. The purpose of this study was to illustrate the early activation of the cell-mediated response in experimental model of TBI. Methods: Lateral fluid percussion injury (LFPI), a TBI model causing both focal cortical lesion and diffuse damage in the ipsilateral hemisphere, was induced in adult male Wistar rats. Sham-operated rats were used as a control group. Animals were sacrificed 1, 3, or 7 days following the procedure. Markers of the cellular arm of adaptive immunity, CD+ cells, were evaluated by quantitative and qualitative immunohistochemical and immunofluorescent analyses of the brain tissue. Results: The results of this study demonstrate the invasion of CD3+, CD4+, and CD8+ cells in the ipsilateral cortices of the brain-injured animals. The number of CD3+ cells significantly increased 1 day after the trauma and has decreased towards the 8th day. Furthermore, CD4+ cells were most abundantly present in the cortex 3 days after the injury. Invasion of CD8+ cells was also noted not only in the cortex but also in the ipsilateral subpial space. Conclusion: Reported results show that LFPI elicits cellular immune response in the first days following TBI, which could modulate secondary events following the trauma and determining recovery outcome. This work was fully supported by project uniri- biomed-18-204 to Prof Gordana Župan.

Introduction: Traumatic brain injury (TBI), being one of the leading causes of death and disabilities worldwide, represents an immense problem from a socio-economical and epidemiological aspect. The adequate neuroprotective therapy that could ameliorate neuroinflammation processes is still lacking and in the focus of the preclinical research. A PPAR-γ agonist, pioglitazone, has been shown to attenuate neuronal damage, cortical loss and microglial activation in some rodent models of TBI. Aim of the study: We investigated whether pioglitazone, administered twice daily, affects the microglial morphology as well as the expression of some microglia activation markers in the parietal cortex and the hippocampus of rats following TBI. Materials and methods: Experiments were performed on adult male Wistar rats divided into three groups. Single moderate lateral fluid percussion injury was carried out over the left parietal cortex. Following the injury, animals were administered with pioglitazone or vehicle in the peritoneal cavity in two doses, first one 10 minutes and second 12 hours after injury. Sham-operated, vehicle-treated animals were used as a control group. Twenty-four hours after the injury induction, animals were sacrificed and their brains were extracted and processed for the immunohistological and the Western blot analyses. Results: Digital reconstruction and the analyses of the cells labeled with microglial- specific marker Iba-1 indicated that the brain trauma caused changes in the cellular morphological features such as the extent of the process branching. The application of the tested drug did not affect these morphological changes. However, our results suggest that pioglitazone caused a decrease in the hippocampal expression of TLR- 2, microglia activation marker. Conclusion: Preliminary results of our study imply that pioglitazone could affect some features of the posttraumatic microglial reaction after TBI in the rat. This work was fully supported by project uniri-biomed-18-204 to Ž.G.

Introduction: One of the leading causes of death and disability throughout the world, traumatic brain injury (TBI), still lacks clinically effective neuroprotective therapy. Previously it was found that, in the TBI in rats, application of a single dose of pioglitazone, a peroxisome proliferator- activated receptor-γ (PPARγ) agonist, had some limited beneficial effects on trauma-induced oxidative hippocampal damage and neurodegeneration. The aim of this study was to examine the effects of pioglitazone, applied twice daily, on the microglial activation and the expressions of inflammation (COX-2) and cell stress (HSP70) markers in the rat hippocampus following lateral fluid percussion injury (LFPI). Materials and methods: Moderate brain trauma was performed over the left parietal cortex by the LFPI method in adult male Wistar rats. Pioglitazone or vehicle were administered i.p. 10 min and 12 h after the injury. Sham- operated, vehicle treated animals were used as the control group. Rats were sacrificed 24 h after TBI and their hippocampi were prepared for the histological and western blotting analyses. Results: Pioglitazone significantly decreased TBI-induced microglial activation in the dentate gyrus of the hippocampus. TBI caused an increase in the expressions of COX-2 and HSP70, but the applied PPARγ agonist did not have an effect on the levels of these proteins. Conclusions: Our study showed that pioglitazone, applied twice daily, reduced microglial reaction in the hippocampus after TBI in the rat, but did not influence the levels of measured inflammatory and cell stress markers. This work was supported by the University of Rijeka, Croatia, project number uniri-biomed- 18-204 to Ž.G.

Aphasia is an acquired language impairment typically caused by stroke. It occurs as a result of damage to specific brain regions, affecting one or more aspects of language. Traumatic brain injury (TBI) is an injury caused by external physical force or violent movement of the head. TBI often results in cognitive, physical, behavioral, and communication difficulties. Discourse analysis, including the study of coherence, can provide information needed to understand the language manifestation of aphasia and TBI. Coherence refers to the ability to maintain thematic unity and semantic connectedness of discourse at the propositional level. The notion of impaired coherence in discourse of people with TBI is widely accepted. On the other hand, there has been considerable debate of whether such deficits exist in discourse of people with aphasia. This research studied the global coherence in narrative discourse of people with aphasia and TBI assuming that no difference would be found. The study included the analysis of transcripts of 6 subjects (3 with aphasia and 3 with TBI). All of them were patients in The Special Hospital for Medical Rehabilitation in Krapinske Toplice. Data analysis was performed in the CLAN, using a 4-point subjective scale to measure global coherence. Statistical data processing was done in IBM SPSS Statistic – version 26 (t-test). No statistically significant difference was found in the coherence of discourse of the participants with aphasia and participants with TBI (p> 0, 05). That confirmed the initial hypothesis. Therefore, it seems possible that different background difficulties are manifested in the same way. In other words, language pathology in people with aphasia and deficits of executive functions in people with TBI both result in impaired narrative organization and production. However, due to a small sample of participants and lack of control of the sociodemographic and clinical factors, caution in generalization of results is needed.