The additive effect of aging on sepsis-induced cognitive impairment and neuroinflammation

Systemic inflammation is emerging as a significant driver of cognitive decline in the aged and vulnerable brain. In sepsis survivors animals low-grade brain inflammation occurs, suggesting that sepsis is able to induce in microglia a primed-like state. The purpose of this study is to analyze the role of sepsis-induced brain inflammation in the progression of the physiological process of brain aging. Wistar rats 2 month-old were subjected to sepsis and 60 and 90 days after were submitted to the new object recognition test and brain was removed to the determination of cytokines, myeloperoxidase (MPO) activity, amyloid-beta peptide (A beta) and immunohistochemistry markers of microglial activation. In the hippocampus, from 60 to 90 days there was an increase in TNF-alpha and IL-1 beta levels in septic animals. This also occurred to the levels of IL-1 beta and IL-6 in the prefrontal cortex. This was associated with persistent increased in microglial activation and A beta levels. In conclusion, neuroinflammation is persistent after sepsis and this could burst the usual inflammation that occurs during brain aging.