Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model

Harboring the behavioral and histopathological signatures of Alzheimer's disease (AD), senescence accelerated mouse-prone 8 (SAMP8) mice are currently considered a robust model for studying AD. However, the underlying mechanisms, prioritized pathways and genes in SAMP8 mice linked to AD remain...

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Main Authors: Cheng, Xiao-rui, Cui, Xiu-liang, Zheng, Yue, Zhang, Gui-rong, Li, Peng, Huang, Huang, Zhao, Yue-ying, Bo, Xiao-chen, Wang, Sheng-qi, Zhou, Wen-xia, Zhang, Yong-xiang
Format: Online
Language:English
Published: Frontiers Media S.A. 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810591/
id pubmed-3810591
recordtype oai_dc
spelling pubmed-38105912013-11-05 Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model Cheng, Xiao-rui Cui, Xiu-liang Zheng, Yue Zhang, Gui-rong Li, Peng Huang, Huang Zhao, Yue-ying Bo, Xiao-chen Wang, Sheng-qi Zhou, Wen-xia Zhang, Yong-xiang Neuroscience Harboring the behavioral and histopathological signatures of Alzheimer's disease (AD), senescence accelerated mouse-prone 8 (SAMP8) mice are currently considered a robust model for studying AD. However, the underlying mechanisms, prioritized pathways and genes in SAMP8 mice linked to AD remain unclear. In this study, we provide a biological interpretation of the molecular underpinnings of SAMP8 mice. Our results were derived from differentially expressed genes in the hippocampus and cerebral cortex of SAMP8 mice compared to age-matched SAMR1 mice at 2, 6, and 12 months of age using cDNA microarray analysis. On the basis of PPI, MetaCore and the co-expression network, we constructed a distinct genetic sub-network in the brains of SAMP8 mice. Next, we determined that the regulation of synaptic transmission and apoptosis were disrupted in the brains of SAMP8 mice. We found abnormal gene expression of RAF1, MAPT, PTGS2, CDKN2A, CAMK2A, NTRK2, AGER, ADRBK1, MCM3AP, and STUB1, which may have initiated the dysfunction of biological processes in the brains of SAMP8 mice. Specifically, we found microRNAs, including miR-20a, miR-17, miR-34a, miR-155, miR-18a, miR-22, miR-26a, miR-101, miR-106b, and miR-125b, that might regulate the expression of nodes in the sub-network. Taken together, these results provide new insights into the biological and genetic mechanisms of SAMP8 mice and add an important dimension to our understanding of the neuro-pathogenesis in SAMP8 mice from a systems perspective. Frontiers Media S.A. 2013-10-29 /pmc/articles/PMC3810591/ /pubmed/24194717 http://dx.doi.org/10.3389/fnagi.2013.00065 Text en Copyright © 2013 Cheng, Cui, Zheng, Zhang, Li, Huang, Zhao, Bo, Wang, Zhou and Zhang. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Cheng, Xiao-rui
Cui, Xiu-liang
Zheng, Yue
Zhang, Gui-rong
Li, Peng
Huang, Huang
Zhao, Yue-ying
Bo, Xiao-chen
Wang, Sheng-qi
Zhou, Wen-xia
Zhang, Yong-xiang
spellingShingle Cheng, Xiao-rui
Cui, Xiu-liang
Zheng, Yue
Zhang, Gui-rong
Li, Peng
Huang, Huang
Zhao, Yue-ying
Bo, Xiao-chen
Wang, Sheng-qi
Zhou, Wen-xia
Zhang, Yong-xiang
Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
author_facet Cheng, Xiao-rui
Cui, Xiu-liang
Zheng, Yue
Zhang, Gui-rong
Li, Peng
Huang, Huang
Zhao, Yue-ying
Bo, Xiao-chen
Wang, Sheng-qi
Zhou, Wen-xia
Zhang, Yong-xiang
author_sort Cheng, Xiao-rui
title Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
title_short Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
title_full Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
title_fullStr Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
title_full_unstemmed Nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an Alzheimer's disease animal model
title_sort nodes and biological processes identified on the basis of network analysis in the brain of the senescence accelerated mice as an alzheimer's disease animal model
description Harboring the behavioral and histopathological signatures of Alzheimer's disease (AD), senescence accelerated mouse-prone 8 (SAMP8) mice are currently considered a robust model for studying AD. However, the underlying mechanisms, prioritized pathways and genes in SAMP8 mice linked to AD remain unclear. In this study, we provide a biological interpretation of the molecular underpinnings of SAMP8 mice. Our results were derived from differentially expressed genes in the hippocampus and cerebral cortex of SAMP8 mice compared to age-matched SAMR1 mice at 2, 6, and 12 months of age using cDNA microarray analysis. On the basis of PPI, MetaCore and the co-expression network, we constructed a distinct genetic sub-network in the brains of SAMP8 mice. Next, we determined that the regulation of synaptic transmission and apoptosis were disrupted in the brains of SAMP8 mice. We found abnormal gene expression of RAF1, MAPT, PTGS2, CDKN2A, CAMK2A, NTRK2, AGER, ADRBK1, MCM3AP, and STUB1, which may have initiated the dysfunction of biological processes in the brains of SAMP8 mice. Specifically, we found microRNAs, including miR-20a, miR-17, miR-34a, miR-155, miR-18a, miR-22, miR-26a, miR-101, miR-106b, and miR-125b, that might regulate the expression of nodes in the sub-network. Taken together, these results provide new insights into the biological and genetic mechanisms of SAMP8 mice and add an important dimension to our understanding of the neuro-pathogenesis in SAMP8 mice from a systems perspective.
publisher Frontiers Media S.A.
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810591/
_version_ 1612021334153363456

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