2018
DOI: 10.3390/ijms19082323
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miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline

Abstract: 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 regu… Show more

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Cited by 28 publications
(16 citation statements)
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“…Among the mechanisms proposed to explain the miR‐34a and miR‐34c effects on memory impairment are the decreased expression of sirtuin‐1 (Bhatnagar et al, 2014; Li et al, 2011). In addition, overexpression of miR‐34c in hippocampal neurons negatively regulated dendritic outgrowth (Kao et al, 2018).…”
Section: Discussionmentioning
confidence: 99%
“…Among the mechanisms proposed to explain the miR‐34a and miR‐34c effects on memory impairment are the decreased expression of sirtuin‐1 (Bhatnagar et al, 2014; Li et al, 2011). In addition, overexpression of miR‐34c in hippocampal neurons negatively regulated dendritic outgrowth (Kao et al, 2018).…”
Section: Discussionmentioning
confidence: 99%
“…Many miRNAs have been identified as key elements for the regulation of cognitive functions and memory processes lost in AD, through the regulation of activity-mediated protein synthesis at the synaptic level (Ramakrishna and Muddashetty, 2019). Mice overexpressing the miR-34c are characterized by reduced dendritic length and spine density (Kao et al, 2018). In an AD mouse model (Tg2576 mice), it was found that miR-124 is dramatically increased in the hippocampus and is directly associated with deficits in synaptic plasticity and memory dysfunction (Wang et al, 2018).…”
Section: Micrornas’ Involvement In Alzheimer’s Diseasementioning
confidence: 99%
“…Moreover, overexpression of miR‐34c perturbs dendritic outgrow and diminishes the number of dendritic spine and filopodia. From the above‐mentioned document, miR‐34c could be considered as a therapeutic target correlating to AD‐linked cognitive deficit (Kao, Wang, & Tsai, 2018). miRNA‐125b is one of the raised miRNAs in the brain of patients with AD.…”
Section: Neurological Disorders Associated With Cognitive Impairmentmentioning
confidence: 99%