AI Article Synopsis

  • Alzheimer's disease (AD) is a neurodegenerative disorder that leads to memory loss and cognitive decline, often with mood changes and confusion, and the search for its causes is focused on the cerebral cortex through analysis of gene expression.
  • A study analyzed RNA expression in the frontal, temporal, and entorhinal cortex of AD patients and found key genes showing significant changes, particularly AEBP1 and COLEC12, which were also assessed in peripheral blood samples of late-onset AD patients.
  • The research connects the up-regulation of AEBP1 and COLEC12 to the TGF-β signaling pathway and suggests these genes could serve as important diagnostic markers for differentiating late-onset AD patients from healthy

Article Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory and cognitive impairment, often accompanied by alterations in mood, confusion, and, ultimately, a state of acute mental disturbance. The cerebral cortex is considered a promising area for investigating the underlying causes of AD by analyzing transcriptional patterns, which could be complemented by investigating blood samples obtained from patients. We analyzed the RNA expression profiles of three distinct areas of the brain cortex, including the frontal cortex (FC), temporal cortex (TC), and entorhinal cortex (EC) in patients with AD. Functional enrichment analysis was performed on the differentially expressed genes (DEGs) across the three regions. The two genes with the most significant expression changes in the EC region were selected for assessing mRNA expression levels in the peripheral blood of late-onset AD patients using quantitative PCR (qPCR). We identified eight shared DEGs in these regions, including AEBP1 and COLEC12, which exhibited prominent changes in expression. Functional enrichment analysis uncovered a significant association of these DEGs with the transforming growth factor-β (TGF-β) signaling pathway and processes related to angiogenesis. Importantly, we established a robust connection between the up-regulation of AEBP1 and COLEC12 in both the brain and peripheral blood. Furthermore, we have demonstrated the potential of AEBP1 and COLEC12 genes as effective diagnostic tools for distinguishing between late-onset AD patients and healthy controls. This study unveils the intricate interplay between AEBP1 and COLEC12 in AD and underscores their potential as markers for disease detection and monitoring.

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Source
http://dx.doi.org/10.1007/s12031-024-02212-8DOI Listing

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