Chronic brain changes caused by severe systemic inflammatory episode

Background Sepsis-associated encephalopathy (SAS) is a neurological complication of severe systemic inflammatory episode that compromises brain function. This impairment can lead to cognitive dysfunction appears precede neurodegenerative disorders such as Alzheimer’s disease. However, the events by which inflammation causes significant damage are not yet fully established. With in mind, this study sought investigate persistent changes after episode. Method Male Wistar rats (90 days old) were divided into two experimental groups: sham (n = 33) and sepsis 37). For induction inflammation, animals underwent cecal ligation perforation (CLP). Animals followed for 30, 60 120 days. In all time-points, we performed object recognition task evaluate declarative memory Western Blotting assess astrocyte-related proteins (GFAP, GLT-1 Mao-B). At 30 days, evaluated ΒBB integrity [cerebrospinal fluid (CSF) albumin levels cellularity HCLP] glucose metabolism (FDG-PET imaging). Result Our results show CLP model compromised long-term at Furthermore, found higher CSF compared (p 0.023) post-sepsis 0.002). addition, also observed an increase induction. We whole hypometabolism (local maxima, t(12) -3.7) t(9) -8.45), suggesting metabolic abnormalities. Finally, proteins. hippocampal (p<0.001) cortical GFAP < 0.0001) immunocontents reduced sham. decreased 0,05) MAO-B 0.01) immunocontents. hippocampus (p<0.05). Conclusion BBB integrity, seems associated with impairment. astrocytes seem be reacting changing their protein expression, typical feature reactive astrocytes.