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A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease
Since the world population is ageing, dementia is going to be a growing concern. Alzheimer’s disease is the most common form of dementia. The pathogenesis of Alzheimer’s disease is extensively studied, yet unknown remains. Therefore, we aimed to extract new knowledge from existing data. We analysed...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239885/ https://www.ncbi.nlm.nih.gov/pubmed/32433480 http://dx.doi.org/10.1038/s41598-020-64452-z |
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author | Hosseinian, Saeedeh Arefian, Ehsan Rakhsh-Khorshid, Hassan Eivani, Mehdi Rezayof, Ameneh Pezeshk, Hamid Marashi, Sayed-Amir |
author_facet | Hosseinian, Saeedeh Arefian, Ehsan Rakhsh-Khorshid, Hassan Eivani, Mehdi Rezayof, Ameneh Pezeshk, Hamid Marashi, Sayed-Amir |
author_sort | Hosseinian, Saeedeh |
collection | PubMed |
description | Since the world population is ageing, dementia is going to be a growing concern. Alzheimer’s disease is the most common form of dementia. The pathogenesis of Alzheimer’s disease is extensively studied, yet unknown remains. Therefore, we aimed to extract new knowledge from existing data. We analysed about 2700 upregulated genes and 2200 downregulated genes from three studies on the CA1 of the hippocampus of brains with Alzheimer’s disease. We found that only the calcium signalling pathway enriched by 48 downregulated genes was consistent between all three studies. We predicted miR-129 to target nine out of 48 genes. Then, we validated miR-129 to regulate six out of nine genes in HEK cells. We noticed that four out of six genes play a role in synaptic plasticity. Finally, we confirmed the upregulation of miR-129 in the hippocampus of brains of rats with scopolamine-induced amnesia as a model of Alzheimer’s disease. We suggest that future research should investigate the possible role of miR-129 in synaptic plasticity and Alzheimer’s disease. This paper presents a novel framework to gain insight into potential biomarkers and targets for diagnosis and treatment of diseases. |
format | Online Article Text |
id | pubmed-7239885 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-72398852020-05-29 A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease Hosseinian, Saeedeh Arefian, Ehsan Rakhsh-Khorshid, Hassan Eivani, Mehdi Rezayof, Ameneh Pezeshk, Hamid Marashi, Sayed-Amir Sci Rep Article Since the world population is ageing, dementia is going to be a growing concern. Alzheimer’s disease is the most common form of dementia. The pathogenesis of Alzheimer’s disease is extensively studied, yet unknown remains. Therefore, we aimed to extract new knowledge from existing data. We analysed about 2700 upregulated genes and 2200 downregulated genes from three studies on the CA1 of the hippocampus of brains with Alzheimer’s disease. We found that only the calcium signalling pathway enriched by 48 downregulated genes was consistent between all three studies. We predicted miR-129 to target nine out of 48 genes. Then, we validated miR-129 to regulate six out of nine genes in HEK cells. We noticed that four out of six genes play a role in synaptic plasticity. Finally, we confirmed the upregulation of miR-129 in the hippocampus of brains of rats with scopolamine-induced amnesia as a model of Alzheimer’s disease. We suggest that future research should investigate the possible role of miR-129 in synaptic plasticity and Alzheimer’s disease. This paper presents a novel framework to gain insight into potential biomarkers and targets for diagnosis and treatment of diseases. Nature Publishing Group UK 2020-05-20 /pmc/articles/PMC7239885/ /pubmed/32433480 http://dx.doi.org/10.1038/s41598-020-64452-z Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Hosseinian, Saeedeh Arefian, Ehsan Rakhsh-Khorshid, Hassan Eivani, Mehdi Rezayof, Ameneh Pezeshk, Hamid Marashi, Sayed-Amir A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title | A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title_full | A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title_fullStr | A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title_full_unstemmed | A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title_short | A meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with Alzheimer’s disease |
title_sort | meta-analysis of gene expression data highlights synaptic dysfunction in the hippocampus of brains with alzheimer’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239885/ https://www.ncbi.nlm.nih.gov/pubmed/32433480 http://dx.doi.org/10.1038/s41598-020-64452-z |
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