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Int. J. Mol. Sci. 2018, 19(8), 2323;

miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline

Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan
Department of Pediatrics, E-Da Hospital, Kaohsiung 824, Taiwan
Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan
Research Center of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan
Author to whom correspondence should be addressed.
Received: 30 June 2018 / Revised: 25 July 2018 / Accepted: 3 August 2018 / Published: 8 August 2018
(This article belongs to the Special Issue Molecular Mechanism of Alzheimer's Disease)
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Microribonucleic acids (miRNAs) play a pivotal role in numerous aspects of the nervous system and are increasingly recognized as key regulators in neurodegenerative diseases. This study hypothesized that miR-34c, a miRNA expressed in mammalian hippocampi whose expression level can alter the hippocampal dendritic spine density, could induce memory impairment akin to that of patients with Alzheimer’s disease (AD) in mice. In this study, we showed that miR-34c overexpression in hippocampal neurons negatively regulated dendritic length and spine density. Hippocampal neurons transfected with miR-34c had shorter dendrites on average and fewer filopodia and spines than those not transfected with miR-34c (control mice). Because dendrites and synapses are key sites for signal transduction and fundamental structures for memory formation and storage, disrupted dendrites can contribute to AD. Therefore, we supposed that miR-34c, through its effects on dendritic spine density, influences synaptic plasticity and plays a key role in AD pathogenesis. View Full-Text
Keywords: miR-34c; dendritic spine; Alzheimer’s disease miR-34c; dendritic spine; Alzheimer’s disease

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Kao, Y.-C.; Wang, I.-F.; Tsai, K.-J. miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline. Int. J. Mol. Sci. 2018, 19, 2323.

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