RESUMO
Breaking time reversal symmetry in a topological insulator may lead to quantum anomalous Hall effect and axion insulator phase. MnBi4Te7 is a recently discovered antiferromagnetic topological insulator with TN â¼ 12.5 K, which is composed of an alternatively stacked magnetic layer (MnBi2Te4) and nonmagnetic layer (Bi2Te3). By means of scanning tunneling spectroscopy, we clearly observe the electronic state present at a step edge of a magnetic MnBi2Te4 layer but absent at nonmagnetic Bi2Te3 layers at 4.5 K. Furthermore, we find that as the temperature rises above TN the edge state vanishes, while the point defect induced state persists upon an increase in temperature. These results confirm the observation of magnetism-induced edge states. Our analysis based on an axion insulator theory reveals that the nontrivial topological nature of the observed edge state.
RESUMO
OBJECTIVES: Long-non-coding RNAs (lncRNAs) have been involved in central nervous system recently. A number of studies have reported that lncRNA NEAT1 exerts critical roles in neurodegenerative disorder. Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) has been reported to exert function in the accumulation of amyloid-ß (Aß). Moreover, BACE1 acts as a target of miR-124 in the progression of AD. So far, the biological role and underlying mechanisms of NEAT1 and miR-124 in AD remains elusive. METHODS: The relative NEAT1 and miR-124 expression was examined by qRT-PCR in the tissues and cells line of AD. Cell apoptosis was examined by FACS. Luciferase reporter assay was performed to verify that miR-124 is a direct target of NEAT1, and BACE1 is a downstream target of miR-124. qRT-PCR and western blot analysis were also performed to determinate the BACE1 and the phosphorylation of tau protein. RESULTS: NEAT1 was notably up-regulated and miR-124 was remarkably down-regulated in AD mouse model. Knockdown of NEAT1 or overexpression of miR-124 showed the protective effects on cellular AD model induced by Aß. Moreover, miR-124 expression could be up- and down-regulated by suppression or overexpression of NEAT1, respectively. In addition, the expression of BACE1 was the potential functional target of miR-124. These findings suggested that NEAT1 might play a vital role in the development of AD by regulating miR-124/BACE1 axis. DISCUSSION: The present study showed that NEAT1 worked as a regulating factor to promote the development of AD via modulating miR-124/BACE1 axis, which might be considered as a novel target in AD treatment.
