Abstract
BackgroundAlzheimer’s disease (AD) is a fatal neurodegenerative disorder, and the lesions originate in the entorhinal cortex (EC) and hippocampus (HIP) at the early stage of AD progression. Gaining insight into the molecular mechanisms underlying AD is critical for the diagnosis and treatment of this disorder. Recent discoveries have uncovered the essential roles of microRNAs (miRNAs) in aging and have identified the potential of miRNAs serving as biomarkers in AD diagnosis.MethodsWe sought to apply bioinformatics tools to investigate microarray profiles and characterize differentially expressed genes (DEGs) in both EC and HIP and identify specific candidate genes and pathways that might be implicated in AD for further analysis. Furthermore, we considered that DEGs might be dysregulated by miRNAs. Therefore, we investigated patients with AD and healthy controls by studying the gene profiling of their brain and blood samples to identify AD-related DEGs, differentially expressed miRNAs (DEmiRNAs), along with gene ontology (GO) analysis, KEGG pathway analysis, and construction of an AD-specific miRNA–mRNA interaction network.ResultsOur analysis identified 10 key hub genes in the EC and HIP of patients with AD, and these hub genes were focused on energy metabolism, suggesting that metabolic dyshomeostasis contributed to the progression of the early AD pathology. Moreover, after the construction of an miRNA–mRNA network, we identified 9 blood-related DEmiRNAs, which regulated 10 target genes in the KEGG pathway.ConclusionsOur findings indicated these DEmiRNAs having the potential to act as diagnostic biomarkers at an early stage of AD.
Highlights
Alzheimer’s disease (AD) is the most frequent cause of dementia, accounting for 60–80% of all such cases [1]
In the molecular function (MF) group, the gene ontology (GO) terms mainly involved in proton-transporting ATPase activity, protein binding, protein complex binding, and androgen receptor binding (Fig. 3C)
KEGG pathway enrichment analysis showed the common DEGs (CDEGs) were mainly enriched in synaptic vesicle cycle, biosynthesis of antibiotics, carbon metabolism, biosynthesis of amino acids, oxidative phosphorylation, and AD (Fig. 3D)
Summary
Alzheimer’s disease (AD) is the most frequent cause of dementia, accounting for 60–80% of all such cases [1]. AD is an age-related progressive neurodegenerative disorder, and the most common type is the late-onset, . Li et al Hereditas (2021) 158:25 referred to as sporadic AD, which is defined as AD with an age-onset > 65 years old, and is ascribed to a complex combination of an individual’s genes, environment, and lifestyle habits. The early-onset AD, called familial AD (FAD), occurs at onset ages ranging from 30–65 years old, and its rarely hereditary involving the amyloid precursor protein, presenilin-1 (PS1), presenilin-2 (PS2) and apolipoprotein E (APOE) ɛ4 allele genes [3, 4]. Alzheimer’s disease (AD) is a fatal neurodegenerative disorder, and the lesions originate in the entorhinal cortex (EC) and hippocampus (HIP) at the early stage of AD progression. Recent discoveries have uncovered the essential roles of microRNAs (miRNAs) in aging and have identified the potential of miRNAs serving as biomarkers in AD diagnosis
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