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Brain & Heart

ORIGINAL RESEARCH ARTICLE
Deciphering molecular atlas of Alzheimer’s

disease: A comprehensive bioinformatic analysis
of gene expression and protein interaction

networks

Shan Luo 1† , Yifei Wang 1† , and Kohji Fukunaga *
2
1 Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of
Tokyo, Kashiwa, Chiba, Japan
2 Department of CNS Drug Innovation, Graduate School of Pharmaceutical Sciences, Tohoku
University, Sendai, Miyagi, Japan

Abstract
Alzheimer’s disease (AD) represents a formidable challenge in the realm of
neurodegenerative research due to its complex pathology. Despite tremendous
scientific endeavors, the intricate molecular underpinnings of AD remain incompletely
understood, necessitating a multidimensional approach to decipher its complexity. In
this study, we analyzed differential gene expression, gene ontology (GO) enrichment,
and protein–protein interaction (PPI) networks using advanced bioinformatics
† These authors contributed equally tools to dissect the molecular landscape of AD. Initially, our research identified 732
to this work.
differentially expressed genes (DEGs), which provided a comprehensive view of the
*Corresponding author: genetic disruptions associated with AD. The results of subsequent GO enrichment
Kohji Fukunaga
(kfukunaga@tohoku.ac.jp) analyses revealed that DEGs were enriched in several critical biological processes,
predominantly including translation, neuroinflammation, and synaptic functionality,
Citation: Luo S, Wang Y, underscoring the multifaceted nature of AD pathology. The PPI network analysis
Fukunaga K. Deciphering molecular
atlas of Alzheimer’s disease: A further unveiled the central role of ribosomal proteins, such as RPL12, RPL15, RPL18,
comprehensive bioinformatic RPL19, RPL27, RPL35, RPL36, RPS16, RPS19, and RPS9, establishing a novel link
analysis of gene expression and between protein synthesis disruptions and the molecular mechanisms of AD. These
protein interaction networks.
Brain & Heart. 2024;2(4):2906. results not only deepen the understanding of molecular mechanisms underlying AD
doi: 10.36922/bh.2906 but also illuminate potential therapeutic pathways and biomarkers for AD. Overall,
Received: February 8, 2024 our comprehensive bioinformatics exploration unraveled the complex molecular
mechanisms that govern AD pathogenesis and highlighted promising new targets
Accepted: May 23, 2024
for the diagnosis and treatment of AD, creating a foundational framework for future
Published Online: August 29, 2024 research on AD.
Copyright: © 2024 Author(s).
This is an Open-Access article
distributed under the terms of the Keywords: Alzheimer’s disease; Differential gene expression; Bioinformatics; Protein–
Creative Commons Attribution protein interaction; Molecular mechanisms
License, permitting distribution,
and reproduction in any medium,
provided the original work is
properly cited.
1. Introduction
Publisher’s Note: AccScience
Publishing remains neutral with Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that not only
regard to jurisdictional claims in
published maps and institutional impairs the cognition and memory of patients but also severely compromises the
affiliations. emotional and physical well-being of patients and family caregivers. As the global

Volume 2 Issue 4 (2024) 1 doi: 10.36922/bh.2906