ArticleMolecular neurobiology2024
Single-Cell RNA Sequencing Transcriptomics Revealed HCMV IE2-Related Microglia Responses in Alzheimer's-Like Disease in Transgenic Mice.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Recent Insights into the Role of Herpesviridae in Alzheimer's Disease: A Structured Narrative Review Based on a Systematic Literature Search.Neurology international · 2026Review
- Human cytomegalovirus infection and cognitive decline: insights from population and experimental studies.Frontiers in aging neuroscience · 2025Review
- Human cytomegalovirus-IE2 suppresses antigen presentation of macrophage through the IL10/STAT3 signalling pathway in transgenic mouse.PloS one · 2025Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Although multiple factors are known to concur with Alzheimer's disease (AD), the relationship between human cytomegalovirus (HCMV) and AD-like disease is unclear. Here, we propose a hypothesis that HCMV immediate-early 2 (IE2) protein promotes microglia activation and thus leads to AD-like disease. We successfully constructed IE2 transgenic mice expressing IE2 in the hippocampus. Single-cell sequencing analysis revealed that IE2 promoted the activation of microglia and upregulated the expression of disease-associated microglia genes. Differentially expressed gene analysis and pathway enrichment revealed that IE2 upregulated immune and nervous system disease-related genes. Immunohistochemical analysis showed that the expressions of both amyloid precursor protein (APP) and p-Tau were significantly upregulated in the brains of IE2 mice and were markers of AD. Taken together, these findings provide useful insights into AD-like disease activated by HCMV IE2.
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Registered trials
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