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Zuhal Yurttaş1, Tugay Çamoğlu1, Ömer Faruk Düzenli1

  • 1Institute of Neurological Sciences, Istanbul University-Cerrahpaşa, Istanbul, Turkey.

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Amyloid beta (Aβ) alters gene expression in a dose-dependent manner, suggesting its role in Alzheimer's Disease (AD) pathogenesis. This study identified key genes affected by Aβ treatments, providing insights into AD molecular mechanisms.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genomics

Background:

  • Amyloid beta (Aβ) acts as a transcriptional regulator, influencing genes involved in its own production and Alzheimer's Disease (AD) pathology.
  • Gene expression alterations are critical in neurodegeneration, particularly in AD.

Purpose of the Study:

  • To identify genes with altered expression in response to varying concentrations (0.1µM and 1µM) of Aβ1-42 using RNA-Sequencing (RNA-Seq).

Main Methods:

  • Neurally differentiated LUHMES cells were treated with Aβ1-42.
  • RNA was isolated, quality-assessed, and used for cDNA library construction and sequencing.
  • RNA-Seq data analysis involved nf-core/RNAseq workflow, DESeq2 for differential gene expression, DAVID for enrichment analysis, and Cytoscape for network analysis.

Main Results:

  • Treatment with 0.1µM Aβ1-42 resulted in 125 differentially expressed genes (DEGs), with NGF, BMP6, and SOX10 identified as top hub genes.
  • Treatment with 1µM Aβ1-42 identified 1608 DEGs, including common hub genes like MUS81, TERT, and MET.
  • Gene expression changes occurred in a dose-dependent manner.

Conclusions:

  • Aβ treatments significantly alter gene expression in a dose-dependent manner, affecting pathways from intracellular signaling to histone acetylation.
  • These findings suggest a potential role for Aβ in driving gene expression changes relevant to AD pathogenesis.
  • The study was supported by TÜBİTAK and Istanbul University-Cerrahpaşa Research Fund.