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Inflammatory gene expression profiling in peripheral blood from patients with Alzheimer's disease reveals key pathways and hub genes with potential diagnostic utility: a preliminary study.

Authors
  • Cardona, Kelly1
  • Medina, Javier1
  • Orrego-Cardozo, Mary1
  • Restrepo de Mejía, Francia1
  • Elcoroaristizabal, Xabier2
  • Naranjo Galvis, Carlos Andrés1
  • 1 Facultad de Salud, Universidad Autónoma de Manizales, Manizales, Caldas, Colombia. , (Colombia)
  • 2 Genetracer Biotech, Madrid, España.
Type
Published Article
Journal
PeerJ
Publisher
PeerJ
Publication Date
Jan 01, 2021
Volume
9
Identifiers
DOI: 10.7717/peerj.12016
PMID: 34484988
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disease caused by central nervous system disorders. Late-onset Alzheimer disease (LOAD) is the most common neurodegenerative disorder worldwide. Differences at the expression level of certain genes, resulting from either genetic variations or environmental interactions, might be one of the mechanisms underlying differential risks for developing AD. Peripheral blood genome transcriptional profiling may provide a powerful and minimally invasive tool for the identification of novel targets beyond Aβ and tau for AD research. This preliminary study explores molecular pathogenesis of LOAD-related inflammation through next generation sequencing, to assess RNA expression profiles in peripheral blood from five patients with LOAD and 10 healthy controls. The analysis of RNA expression profiles revealed 94 genes up-regulated and 147 down-regulated. Gene function analysis, including Gene Ontology (GO) and KOBAS-Kyoto Encyclopedia of DEGs and Genomes (KEGG) pathways indicated upregulation of interferon family (INF) signaling, while the down-regulated genes were mainly associated with the cell cycle process. KEGG metabolic pathways mapping showed gene expression alterations in the signaling pathways of JAK/STAT, chemokines, MAP kinases and Alzheimer disease. The results of this preliminary study provided not only a comprehensive picture of gene expression, but also the key processes associated with pathology for the regulation of neuroinflammation, to improve the current mechanisms to treat LOAD. ©2021 Cardona et al.

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