Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease
Pathogenic aging is regarded as asymptomatic AD when there is no cognitive deficit except for neuropathology consistent with Alzheimer's disease. These individuals are highly susceptible to developing AD. Braak and Braak's theory specific to tau pathology illustrates that the brain's...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-07-01
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| Series: | Frontiers in Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnins.2022.966877/full |
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| author | Ankita Kumari Ankita Kumari Ankita Kumari Abdul Rahaman Abdul Rahaman Abdul Rahaman Xin-An Zeng Xin-An Zeng Xin-An Zeng Muhammad Adil Farooq Yanyan Huang Runyu Yao Runyu Yao Murtaza Ali Murtaza Ali Murtaza Ali Romana Ishrat Rafat Ali |
| author_facet | Ankita Kumari Ankita Kumari Ankita Kumari Abdul Rahaman Abdul Rahaman Abdul Rahaman Xin-An Zeng Xin-An Zeng Xin-An Zeng Muhammad Adil Farooq Yanyan Huang Runyu Yao Runyu Yao Murtaza Ali Murtaza Ali Murtaza Ali Romana Ishrat Rafat Ali |
| author_sort | Ankita Kumari |
| collection | DOAJ |
| description | Pathogenic aging is regarded as asymptomatic AD when there is no cognitive deficit except for neuropathology consistent with Alzheimer's disease. These individuals are highly susceptible to developing AD. Braak and Braak's theory specific to tau pathology illustrates that the brain's temporal cortex region is an initiation site for early AD progression. So, the hub gene analysis of this region may reveal early altered biological cascades that may be helpful to alleviate AD in an early stage. Meanwhile, cognitive processing also drags its attention because cognitive impairment is the ultimate result of AD. Therefore, this study aimed to explore changes in gene expression of aged control, asymptomatic AD (AsymAD), and symptomatic AD (symAD) in the temporal cortex region. We used microarray data sets to identify differentially expressed genes (DEGs) with the help of the R programming interface. Further, we constructed the protein-protein interaction (PPI) network by performing the STRING plugin in Cytoscape and determined the hub genes via the CytoHubba plugin. Furthermore, we conducted Gene Ontology (GO) enrichment analysis via Bioconductor's cluster profile package. Resultant, the AsymAD transcriptome revealed the early-stage changes of glutamatergic hyperexcitability. Whereas the connectivity of major hub genes in this network indicates a shift from initially reduced rRNA biosynthesis in the AsymAD group to impaired protein synthesis in the symAD group. Both share the phenomenon of breaking tight junctions and others. In conclusion, this study offers new understandings of the early biological vicissitudes that occur in the brain before the manifestation of symAD and gives new promising therapeutic targets for early AD intervention. |
| first_indexed | 2024-04-13T20:19:04Z |
| format | Article |
| id | doaj.art-3e175d313e6944779dca4e0b16b2652e |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-04-13T20:19:04Z |
| publishDate | 2022-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-3e175d313e6944779dca4e0b16b2652e2022-12-22T02:31:36ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2022-07-011610.3389/fnins.2022.966877966877Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's DiseaseAnkita Kumari0Ankita Kumari1Ankita Kumari2Abdul Rahaman3Abdul Rahaman4Abdul Rahaman5Xin-An Zeng6Xin-An Zeng7Xin-An Zeng8Muhammad Adil Farooq9Yanyan Huang10Runyu Yao11Runyu Yao12Murtaza Ali13Murtaza Ali14Murtaza Ali15Romana Ishrat16Rafat Ali17School of Food Science and Engineering, South China University of Technology, Guangzhou, ChinaGuangdong Key Laboratory of Food Intelligent Manufacturing, Foshan University, Foshan, ChinaOverseas Expertise Introduction Centre for Discipline Innovation of Food Nutrition and Human Health (111 Centre), Guangzhou, ChinaSchool of Food Science and Engineering, South China University of Technology, Guangzhou, ChinaGuangdong Key Laboratory of Food Intelligent Manufacturing, Foshan University, Foshan, ChinaOverseas Expertise Introduction Centre for Discipline Innovation of Food Nutrition and Human Health (111 Centre), Guangzhou, ChinaSchool of Food Science and Engineering, South China University of Technology, Guangzhou, ChinaGuangdong Key Laboratory of Food Intelligent Manufacturing, Foshan University, Foshan, ChinaOverseas Expertise Introduction Centre for Discipline Innovation of Food Nutrition and Human Health (111 Centre), Guangzhou, ChinaInstitute of Food Science and Technology, Khwaja Fareed University of Engineering and Information Technology, Rahim Yar Khan, PakistanGuangdong Key Laboratory of Food Intelligent Manufacturing, Foshan University, Foshan, ChinaSchool of Food Science and Engineering, South China University of Technology, Guangzhou, ChinaOverseas Expertise Introduction Centre for Discipline Innovation of Food Nutrition and Human Health (111 Centre), Guangzhou, ChinaSchool of Food Science and Engineering, South China University of Technology, Guangzhou, ChinaGuangdong Key Laboratory of Food Intelligent Manufacturing, Foshan University, Foshan, ChinaOverseas Expertise Introduction Centre for Discipline Innovation of Food Nutrition and Human Health (111 Centre), Guangzhou, ChinaCenter for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, IndiaCenter for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, IndiaPathogenic aging is regarded as asymptomatic AD when there is no cognitive deficit except for neuropathology consistent with Alzheimer's disease. These individuals are highly susceptible to developing AD. Braak and Braak's theory specific to tau pathology illustrates that the brain's temporal cortex region is an initiation site for early AD progression. So, the hub gene analysis of this region may reveal early altered biological cascades that may be helpful to alleviate AD in an early stage. Meanwhile, cognitive processing also drags its attention because cognitive impairment is the ultimate result of AD. Therefore, this study aimed to explore changes in gene expression of aged control, asymptomatic AD (AsymAD), and symptomatic AD (symAD) in the temporal cortex region. We used microarray data sets to identify differentially expressed genes (DEGs) with the help of the R programming interface. Further, we constructed the protein-protein interaction (PPI) network by performing the STRING plugin in Cytoscape and determined the hub genes via the CytoHubba plugin. Furthermore, we conducted Gene Ontology (GO) enrichment analysis via Bioconductor's cluster profile package. Resultant, the AsymAD transcriptome revealed the early-stage changes of glutamatergic hyperexcitability. Whereas the connectivity of major hub genes in this network indicates a shift from initially reduced rRNA biosynthesis in the AsymAD group to impaired protein synthesis in the symAD group. Both share the phenomenon of breaking tight junctions and others. In conclusion, this study offers new understandings of the early biological vicissitudes that occur in the brain before the manifestation of symAD and gives new promising therapeutic targets for early AD intervention.https://www.frontiersin.org/articles/10.3389/fnins.2022.966877/fullmicroarrayAlzheimersymptomaticasymptomaticgenes |
| spellingShingle | Ankita Kumari Ankita Kumari Ankita Kumari Abdul Rahaman Abdul Rahaman Abdul Rahaman Xin-An Zeng Xin-An Zeng Xin-An Zeng Muhammad Adil Farooq Yanyan Huang Runyu Yao Runyu Yao Murtaza Ali Murtaza Ali Murtaza Ali Romana Ishrat Rafat Ali Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease Frontiers in Neuroscience microarray Alzheimer symptomatic asymptomatic genes |
| title | Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease |
| title_full | Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease |
| title_fullStr | Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease |
| title_full_unstemmed | Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease |
| title_short | Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease |
| title_sort | temporal cortex microarray analysis revealed impaired ribosomal biogenesis and hyperactivity of the glutamatergic system an early signature of asymptomatic alzheimer s disease |
| topic | microarray Alzheimer symptomatic asymptomatic genes |
| url | https://www.frontiersin.org/articles/10.3389/fnins.2022.966877/full |
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