Abstract
Alzheimer’s disease (AD) and diabetes mellitus (DM) are known to have a shared molecular mechanism. We aimed to identify shared blood transcriptomic signatures between AD and DM. Blood expression datasets for each disease were combined and a co-expression network was used to construct modules consisting of genes with similar expression patterns. For each module, a gene regulatory network based on gene expression and protein-protein interactions was established to identify hub genes. We selected one module, where COPS4, PSMA6, GTF2B, GTF2F2, and SSB were identified as dysregulated transcription factors that were common between AD and DM. These five genes were also differentially co-expressed in disease-related tissues, such as the brain in AD and the pancreas in DM. Our study identified gene modules that were dysregulated in both AD and DM blood samples, which may contribute to reveal common pathophysiology between two diseases.
Highlights
Alzheimer’s disease (AD), the most common form of dementia, has pathophysiological characteristics that include amyloid plaques, which are extracellular deposits of beta-amyloid (Aβ) in the brain parenchyma; cerebral amyloid angiopathy, which is the accumulation of Aβ in the cerebral blood vessels; and neurofibrillary tangles, which are deposits of hyper-phosphorylated tau protein inside neurons [1]
Recent evidence has suggested that AD is a brain-specific disease and a systemic disorder associated with inflammation, obesity, and other chronic diseases [2]
We examined whether blood expression values of different datasets from the same disease were correlated with each other
Summary
Alzheimer’s disease (AD), the most common form of dementia, has pathophysiological characteristics that include amyloid plaques, which are extracellular deposits of beta-amyloid (Aβ) in the brain parenchyma; cerebral amyloid angiopathy, which is the accumulation of Aβ in the cerebral blood vessels; and neurofibrillary tangles, which are deposits of hyper-phosphorylated tau protein inside neurons [1]. Recent evidence has suggested that AD is a brain-specific disease and a systemic disorder associated with inflammation, obesity, and other chronic diseases [2]. Substantial epidemiologic studies have reported that diabetes mellitus (DM) is a crucial risk factor for AD [3,4]. Huang et al [3] analyzed approximately 140,000 members of the Taiwanese population and reported that newly diagnosed patients with type 2 DM (T2D) have an increased risk of AD. A study analyzing the Hisayama cohort suggested that. DM is a significant risk factor for all-cause dementia and AD [4]. Several studies based on whole transcriptome analysis have identified a common pathogenesis between AD and DM
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