| Summary: | <p><strong>Background</strong> Brain-derived neurotrophic factor (BDNF) plays a crucial role in the pathogenesis of Alzheimer's disease (AD). MicroRNA (miRNA)-132, which is widely expressed in neurons, is involved in BDNF-mediated neural development by regulating the expression of target gene. This study aims to investigate the effect of miRNA-132 on BDNF and its neuroprotective effect. <strong>Methods</strong> The hippocampal neurons were transfected by miRNA-132 after 72 h in vitro, then exposed to amyloid β-protein (Aβ) on the 7th day to build AD models. The difference of miRNA-132 expression between AD group and control group was detected by real-time fluorescent quantitative polymerase chain reaction (PCR). The alterations of BDNF mRNA were observed in the neurons of different groups. Finally, the cell viability was observed by methyl thiazolyl tetrazolium (MTT) assay in AD neurons transfected with miRNA-132 or incubated with BDNF. Results 1) MiRNA-132 was significantly decreased (<em>t</em> = 13.888, <em>P</em> = 0.000), and the expression of BDNF mRNA was also reduced in AD group (<em>t</em> = -12.274, <em>P</em> = 0.000). 2) Green fluorescence was clearly visible by inverted phase-contrast fluorescence microscopy after transfected with miRNA-132. BDNF mRNA was upregulated when miRNA-132 overexpression both in control group (<em>t</em> = 16.135, <em>P</em> = 0.000) and AD group (<em>t</em> = 8.656, <em>P</em> = 0.000). 3) Cell viability was obviously decreased in neurons exposed to Aβ (<em>t</em> = -6.023, <em>P</em> = 0.000), which was improved when transfected with miRNA-132 (<em>t</em> = 3.385, <em>P</em> = 0.007) or incubated with BDNF (<em>t</em> = 3.672, <em>P</em> = 0.004). <strong>Conclusions </strong>The expression of miRNA-132 and BDNF was reduced in neuronal AD model. MiRNA-132 played an important role on neuroprotection against A β-induced neuronal damage via upregulation of BDNF. It could be expected to provide new perspective for the diagnosis and treatment of AD.</p><p> </p><p><strong>DOI: </strong>10.3969/j.issn.1672-6731.2016.07.009</p>
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