AUTHOR=Fan Chunying , Wu Qi , Ye Xiaoyang , Luo Hongxue , Yan Dongdong , Xiong Yi , Zhu Haili , Diao Yarui , Zhang Wei , Wan Jun TITLE=Role of miR-211 in Neuronal Differentiation and Viability: Implications to Pathogenesis of Alzheimer’s Disease JOURNAL=Frontiers in Aging Neuroscience VOLUME=8 YEAR=2016 URL=https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2016.00166 DOI=10.3389/fnagi.2016.00166 ISSN=1663-4365 ABSTRACT=

Alzheimer’s disease (AD) is an age-related irreversible neurodegenerative disorder characterized by extracellular β Amyloid(Aβ) deposition, intracellular neurofibrillary tangles and neuronal loss. The dysfunction of neurogenesis and increased degeneration of neurons contribute to the pathogenesis of AD. We now report that miR-211-5p, a small non-coding RNA, can impair neurite differentiation by directly targeting NUAK1, decrease neuronal viability and accelerate the progression of Aβ-induced pathologies. In this study, we observed that during embryonic development, the expression levels of miR-211-5p were down-regulated in the normal cerebral cortexes of mice. However, in APPswe/PS1ΔE9 double transgenic adult mice, it was up-regulated from 9 months of age compared to that of the age-matched wild type mice. Studies in primary cortical neuron cultures demonstrated that miR-211-5p can inhibit neurite growth and branching via NUAK1 repression and decrease mature neuron viability. The impairments were more obvious under the action of Aβ. Our data showed that miR-211-5p could inhibit cortical neuron differentiation and survival, which may contribute to the synaptic failure, neuronal loss and cognitive dysfunction in AD.