ArticleFrontiers in neuroscience2022
Temporal Cortex Microarray Analysis Revealed Impaired Ribosomal Biogenesis and Hyperactivity of the Glutamatergic System: An Early Signature of Asymptomatic Alzheimer's Disease.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Profiling lamina specific pyramidal neurons using postmortem human formalin fixed paraffin embedded frontal cortex tissue in combination with digital spatial profiling.Journal of neuroscience methods · 2025Article
- AUGMENTED DOUBLY ROBUST POST-IMPUTATION INFERENCE FOR PROTEOMIC DATA.The annals of applied statistics · 2025Article
- AUGMENTED DOUBLY ROBUST POST-IMPUTATION INFERENCE FOR PROTEOMIC DATA.bioRxiv : the preprint server for biology · 2025Article
- A Map of Transcriptomic Signatures of Different Brain Areas in Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Longitudinal APOE4- and amyloid-dependent changes in the blood transcriptome in cognitively intact older adults.Alzheimer's research & therapy · 2023Article
- Predicting Key Genes and Therapeutic Molecular Modelling to Explain the Association betweenInternational journal of molecular sciences · 2023Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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