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Cerebral transcriptome analysis reveals age-dependent progression of neuroinflammation in P301S mutant tau transgenic male mice

Kim, Joonki, Selvaraji, Sharmelee, Kang, Sung Wook, Lee, Wei Thye, Chen, Christopher Li-Hsian, Choi, Hyungwon, Koo, Edward H., Jo, Dong-Gyu, Leong Lim, Kah, Lim, Yun-An, Arumugam, Thiruma V.·2019·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2019.04.011
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Abstract

Aggregation of the microtubule-associated protein, tau, can lead to neurofibrillary tangle formation in neurons and glia which is the hallmark of tauopathy. The cellular damage induced by the formation of neurofibrillary tangles leads to neuroinflammation and consecutive neuronal death. However, detailed observation of transcriptomic changes under tauopathy together with the comparison of age-dependent progression of neuroinflammatory gene expressions mediated by tau overexpression is required. Employing RNA sequencing on PS19 transgenic mice that overexpress human mutant tau harboring the P301S mutation, we have examined the effects of age-dependent tau overexpression on transcriptomic changes of immune and inflammatory responses in the cerebral cortex. Compared to age-matched wild type control, P301S transgenic mice exhibit significant transcriptomic alterations. We have observed age-dependent neuroinflammatory gene expression changes in both wild type and P301S transgenic mice where tau overexpression further promoted the expression of neuroinflammatory genes in 10-month old P301S transgenic mice. Moreover, functional gene network analyses (gene ontology and pathway enrichment) and prospective target protein interactions predicted the potential involvement of multiple immune and inflammatory pathways that may contribute to tau-mediated neuronal pathology. Our current study on P301S transgenic mice model revealed for the first time, the differences of gene expression patter…

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  • We identified an exaggerated inflammatory gene signature characterized by GO terms such as "positive regulation of cytokine production," "leukocyte activation," and "inflammatory response."

    “In agreement with a previous report (Kim et al., 2019), we identified an exaggerated inflammatory gene signature characterized by GO terms such as “positive regulation of cytokine production,” “leukocyte activation,” and “inflammatory response.””

    From Cholesterol 25-hydroxylase mediates neuroinflammation and neurodegeneration in a mouse model of tauopathy (2024) · cites this paper as Kim et al., 2019

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Metadata

Authors
Kim, J., Selvaraji, S., Kang, S. W., Lee, W. T., Chen, C. L.-H., Choi, H., Koo, E. H., Jo, D.-G., Leong Lim, K., Lim, Y.-A., & Arumugam, T. V.
ORCID
Choi, Hyungwon
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2019-08
Volume
80
Pages
344-357
ISSN
0889-1591
DOI
10.1016/j.bbi.2019.04.011
Cited by
20
References
10
Language
en
Licence
Funders
National Medical Research Council (NMRC-CBRG-0102/2016, GSE118473)

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