miRNA-34c Overexpression Causes Dendritic Loss and Memory Decline
| Autor: | Yu-Chia Kao, Kuen Jer Tsai, I-Fang Wang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Nervous system Dendritic spine Dendritic Spines Biology Hippocampal formation Hippocampus Catalysis Article Inorganic Chemistry lcsh:Chemistry 03 medical and health sciences Mice 0302 clinical medicine Alzheimer Disease Memory Neuroplasticity medicine Animals Humans Physical and Theoretical Chemistry Molecular Biology lcsh:QH301-705.5 Spectroscopy Neurons Memory Disorders Neuronal Plasticity dendritic spine Organic Chemistry General Medicine medicine.disease Computer Science Applications MicroRNAs 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation lcsh:Biology (General) lcsh:QD1-999 Synaptic plasticity Synapses Signal transduction Alzheimer's disease miR-34c Neuroscience Filopodia Alzheimer’s disease 030217 neurology & neurosurgery |
| Zdroj: | International Journal of Molecular Sciences, Vol 19, Iss 8, p 2323 (2018) International Journal of Molecular Sciences Volume 19 Issue 8 |
| ISSN: | 1422-0067 |
| Popis: | 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&rsquo 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. |
| Databáze: | OpenAIRE |
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