MicroRNA-511-3p regulates Aβ1–40 induced decreased cell viability and serves as a candidate biomarker in Alzheimer's disease

Alzheimer's disease (AD) is a progressive neurodegenerative disease with high incidence in the elderly population. MicroRNAs have been reported to abnormally expressed in patients with AD. In this study, we investigated the role of inflammation-related miR-511-3p in AD patients and AD cell models. The level of miR-511-3p was quantified by Real-Time PCR. The diagnostic value was evaluated by receiver operating characteristic curve (ROC) analysis. The correlation between miR-511-3p expression levels and ini-mental state examination (MMSE) scores, Montreal Cognitive Assessment (MoCA) scores and inflammatory factors was analyzed. The concentrations of IL-1β, IL-6 and TNF-α were measured by Enzyme-Linked Immunosorbent Assay (ELISA) in AD cell model and serum from AD patients. Serum miR-511-3p expression was decreased in AD patients and correlated with MMSE score, MoCA score and inflammatory response. MiR-511-3p mimics significantly reversed the effects of Aβ 1–40 on inflammation in AD cells. ROC curve results showed that miR-511-3p had high diagnostic accuracy in distinguishing normal controls from AD patients. Our results show that miR-511-3p is down-regulated in AD patients and has high diagnostic value. MiR-511-3p may participate in the development of AD by regulating the levels of neuroinflammatory factors in AD cells. MiR-511-3p may provide a new perspective for the prevention and pathogenesis of AD.