miRNA-34c overexpression causes dendritic loss and memory decline

Yu Chia Kao, I. Fang Wang, Kuen-Jer Tsai

研究成果: Article

2 引文 (Scopus)

摘要

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.

原文English
文章編號2323
期刊International journal of molecular sciences
19
發行號8
DOIs
出版狀態Published - 2018 八月 8

指紋

Dendritic Spines
spine
Memory Disorders
Dendrites
MicroRNAs
Alzheimer Disease
dendrites
Data storage equipment
Neurons
causes
neurons
Neurodegenerative diseases
mice
Signal transduction
Pseudopodia
Neuronal Plasticity
Neurology
hippocampus
nervous system
synapses

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

引用此文

@article{3c6a8090da664fdd98069ce324f70559,
title = "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 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.",
author = "Kao, {Yu Chia} and Wang, {I. Fang} and Kuen-Jer Tsai",
year = "2018",
month = "8",
day = "8",
doi = "10.3390/ijms19082323",
language = "English",
volume = "19",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "8",

}

miRNA-34c overexpression causes dendritic loss and memory decline. / Kao, Yu Chia; Wang, I. Fang; Tsai, Kuen-Jer.

於: International journal of molecular sciences, 卷 19, 編號 8, 2323, 08.08.2018.

研究成果: Article

TY - JOUR

T1 - miRNA-34c overexpression causes dendritic loss and memory decline

AU - Kao, Yu Chia

AU - Wang, I. Fang

AU - Tsai, Kuen-Jer

PY - 2018/8/8

Y1 - 2018/8/8

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85052158449&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85052158449&partnerID=8YFLogxK

U2 - 10.3390/ijms19082323

DO - 10.3390/ijms19082323

M3 - Article

VL - 19

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 8

M1 - 2323

ER -