Resumo

Introduction: Significant changes in society and in morbidmortality patterns of population are consequences of the process of population aging. As a consequence, the impact of chronic-degenerative diseases is inevitable, specially the dementia syndromes. The main dementia syndrome is Alzheimer Disease (AD), which prevalence has been progressively rising with the population age increasing. The neuroinflamatory component is inherent to AD. The IL-1á is a key cytokine in the inflammation pathway and it is mainly produced by monocytes. The inflammation that occurs in Alzheimer patients’ brains contribute to the neurodegenerative damage, and the increased peripheral levels of inflammatory cytokines are directly correlated with a decline in cognitive symptoms (Holmes et al., 2009). Because of the accessibility limitations of human central nervous cells as research model, peripheral biomarkers are important to follow DA development in patients. Aim: The main issue of this work is to study the expression of IL-1á from circulating monocytes of AD patients. We performed comparative analysis among patients with clinic prodrome conditions - Depression Late-Onset (DLO) - Mild Cognitive Imtpaiment (MCI) - with other dementia - Fronto-Temporal Dementia (FTD) - and with the AD patients that have behavioral symptoms (BPSD). Elderly with no dementia nor depression symptoms were used as control. Methods: We separated the peripheral blood mononuclear cells (PBMC) from patients and controls, which were cultured with or without Lypopolysacaride (LPS) for 18 hours. Afterwards, the cells were harvested and immunoassayed with anti-CD4/FITC and IL-1á/PE, fixed with phormadehyde 2% and acquired by a flow cytometer (Guava/GE). The results were analysed by Cytosoft software statistics analysis were performed using ANOVA (Kruskal-Wallis) by GraphPadPrism. Results: We observed two distinct AD patient groups: (1) a group of patients with similar levels of IL-1á in CD14+ monocytes to control group and (2) a group of patients with increase levels of IL-1á in CD14+ monocytes compared to control group. Furthermore, we showed an increase in the levels of IL-1á in monocytes after LPS stimulation in culture. However, we observed that a group of AD patients did not show an increased of IL-1á levels after stimulation. Conclusion: IL-1á might have a role in AD. More investigation is needed to characterize the AD group of patients that express low levels of peripheral IL-1á with or without stimulus and understand which could be the relation with the AD. Conflict of interest: There is none. Apoio financeiro: INCT, CNPq, CAPES, AMBRIEX, John Simon Guggehnheim Foundation, FAPEMIG