Abstract
We did a comparative analysis of the gene expression profiles of the hippocampus from sleep deprivation and Alzheimer’s disease (AD) mice. Differentially expressed genes (DEGs) were identified by comparing the transcriptome profiles of the hippocampus of sleep deprivation or AD mouse models to matched controls. The common DEGs between sleep deprivation and AD were identified by the overlapping analysis, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The results showed that a total of 16 common DEGs showed similar change patterns in both sleep deprivation mice and AD mice. Sgk1, Ly6a, Atp6v0e, Hspb8, Htra1, Pdk4, Pfkfb3, Golm1, and Plin3 were up-regulated in the two disorders, whereas, Marcksl1, Fgd1, Scarb1, Mvd, Klhl13, Elovl2, and Vps29 were down-regulated. Acetyl-CoA metabolic process and lipid biosynthetic process were significantly enriched by those DEGs. The highly expressed DEGs and the two GO terms were associated with neuropathological changes according to the previous studies. As expected, sleep deprivation may contribute the AD development through these common DEGs.
Highlights
Alzheimer’s disease (AD), a common age-related progressive neurodegenerative disease, is characterized by progressive neuronal loss in the hippocampus and cortex, with the accumulation in the brain of extracellular neuritic plaques caused by b-amyloid (Ab) peptides as well as intracellular neurofibrillary tangles induced by hyperphosphorylated tau proteins, resulting in irreversible memory loss and declined cognitive functioning (Chen et al, 2017; Area-Gomez et al, 2018)
We performed acomparative analysis of the transcriptome profiles of mouse hippocampus of sleep deprivation or AD and identified the common Differentially expressed genes (DEGs) between them, which were highly related to acetyl-CoA metabolic process and lipid biosynthetic process
These common DEGs may explain the potential mechanism of how sleep deprivation affecting AD development
Summary
Alzheimer’s disease (AD), a common age-related progressive neurodegenerative disease, is characterized by progressive neuronal loss in the hippocampus and cortex, with the accumulation in the brain of extracellular neuritic plaques caused by b-amyloid (Ab) peptides as well as intracellular neurofibrillary tangles induced by hyperphosphorylated tau proteins, resulting in irreversible memory loss and declined cognitive functioning (Chen et al, 2017; Area-Gomez et al, 2018). GSE33302 dataset included gene expression data of hippocampus from sleep deprivation mice and time-matched non-sleep-deprived control mice.
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