Neurons and Astrocytes Elicit Brain Region Specific Transcriptional Responses to Prion Disease in the Murine CA1 and Thalamus
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Progressive dysfunction and loss of neurons ultimately culminates in the symptoms and eventual fatality of prion disease, yet the pathways and mechanisms that lead to neuronal degeneration remain elusive. Here, we used RNAseq to profile transcriptional changes in microdissected CA1 and thalamus brain tissues from prion infected mice. Numerous transcripts were altered during clinical disease, whereas very few transcripts were reliably altered at pre-clinical time points. Prion altered transcripts were assigned to broadly defined brain cell types and we noted a strong transcriptional signature that was affiliated with reactive microglia and astrocytes. While very few neuronal transcripts were common between the CA1 and thalamus, we described transcriptional changes in both regions that were related to synaptic dysfunction. Using transcriptional profiling to compare how different neuronal populations respond during prion disease may help decipher mechanisms that lead to neuronal demise and should be investigated with greater detail.
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While microglia expression profiles change considerably over the course of disease in a region-dependent manner, neuronal phenotypes remain comparatively stable.
“Interestingly, while microglia expression profiles changed considerably of the course of disease in a region-dependent manner, neuronal phenotypes remained comparatively stable [37,38].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [37]
Progressive dysregulation of glia cells including microglia can be demonstrated on the gene expression level.
“Progressive dysregulation of glia cells including microglia could also be demonstrated on the gene expression level using novel techniques [37,38].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [37]
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Ghatak, K., Yin, G. N., Choi, M. J., Limanjaya, A., Minh, N. N., Ock, J., Song, K., Kang, D. H., Kwon, Y., Kim, H. M., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-17862-5 · Cited by 17 · see citing works
Palmitoylated Proteins in Dendritic Spine Remodeling
Albanesi, J. P., Baryłko, B., Demartino, G., & Jameson, D. M. (2020) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2020.00022 · Cited by 13 · see citing works
Seweryn, M. T., Pietrzak, M., & Ma, Q. (2020) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2020.05.005 · Cited by 12 · see citing works
Knockdown of the ADHD Candidate Gene Diras2 in Murine Hippocampal Primary Cells
Grünewald, L., Chiocchetti, A. G., Weber, H., Scholz, C. J., Schartner, C., Freudenberg, F., & Reif, A. (2019) · Journal of Attention Disorders · doi:10.1177/1087054718822129 · Cited by 8 · see citing works
In Situ Temporospatial Characterization of the Glial Response to Prion Infection
Michael, A. V., Greenlee, J. J., Harm, T. A., Moore, S. J., Zhang, M., Lind, M. S., Greenlee, M. H. W., & Smith, J. D. (2019) · Veterinary Pathology · doi:10.1177/0300985819861708 · Cited by 6 · see citing works
Complete Microglia Deficiency Accelerates Prion Disease Without Enhancing CNS Prion AccumulationPreprint
Bradford, B. M., McGuire, L. I., Hume, D. A., Pridans, C., & Mabbott, N. A. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3761455 · Cited by 5 · see citing works
Feng, B., Freitas, A. E., Tian, R., Lee, Y. R., Grewal, A. S., Wang, J., & Zou, Y. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.09.09.273011 · Cited by 3 · see citing works
Devotta, A., Hong, C., & Saint‐Jeannet, J. (2018) · doi:10.7554/elife.34404.025 · Cited by 1 · see citing works
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Slota, J. A., Sajesh, B. V., Frost, K. F., Medina, S. J., & Booth, S. A. (2022) · Acta Neuropathologica Communications · doi:10.1186/s40478-022-01450-4 · Cited by 26 · see citing works
Self-citationLoss of Homeostatic Microglia Signature in Prion Diseases
Wang, Y., Hartmann, K., Thies, E., Mohammadi, B., Altmeppen, H., Sepulveda-Falla, D., Glatzel, M., & Krasemann, S. (2022) · Cells · doi:10.3390/cells11192948 · Cited by 12 · see citing works
“Progressive dysregulation of glia cells including microglia could also be demonstrated on the gene expression level using novel techniques [37,38].”
BackgroundMethodCellular Prion Protein and Amyloid-β Oligomers in Alzheimer’s Disease—Are There Connections?
Fułek, M., Hachiya, N., Gachowska, M., Beszłej, J. A., Bartoszewska, E., Kurpas, D., Kurpiński, T., Adamska, H., Poręba, R., Urban, S., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26052097 · Cited by 12 · see citing works
Challenges and Discoveries in Polypharmacology of Neurodegenerative Diseases
Scotti, L., Rodrigues, T. C. M. L., de Sousa, N. F., dos Santos, A. M. F., Guimarães, R. D. A., & Scotti, M. T. (2023) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026623666230126112628 · Cited by 11 · see citing works
Slota, J. A., Lamoureux, L., Frost, K. L., Sajesh, B. V., & Booth, S. A. (2024) · Nature Communications · doi:10.1038/s41467-024-54579-2 · Cited by 8 · see citing works
Self-citationDimitriadis, A., Zhang, F., Murphy, T., Trainer, T., Jaunmuktane, Z., Schmidt, C., Nazari, T., Linehan, J. M., Brandner, S., Collinge, J., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.09.13.507650 · Cited by 8 · see citing works
Reactive astrocytes in prion diseases: Friend or foe?
Makarava, N., Kushwaha, R., & Baskakov, I. V. (2024) · PLoS Pathogens · doi:10.1371/journal.ppat.1012286 · Cited by 6 · see citing works
GeneSetCart: assembling, augmenting, combining, visualizing, and analyzing gene sets
Marino, G. B., Olaiya, S., Evangelista, J. E., Clarke, D. J. B., & Ma’ayan, A. (2025) · GigaScience · doi:10.1093/gigascience/giaf025 · Cited by 6 · see citing works
The Role of Glial Cells in Neurobiology and Prion Neuropathology
Hay, A. J. D., Popichak, K. A., Moreno, J. A., & Zabel, M. D. (2024) · Cells · doi:10.3390/cells13100832 · Cited by 5 · see citing works
Genetic and epigenetic drivers of neurodegenerative disorders
Roy, K., Syed, M., Narad, P., & Sengupta, A. (2025) · Progress in brain research · doi:10.1016/bs.pbr.2025.08.002 · Cited by 5 · see citing works
Slota, J. A., Lamoureux, L., Myskiw, J., Frost, K. L., Medina, S. J., Kielich, D. M. S., Leonhardt, M., Thapar, G., Bailey-Elkin, B. A., & Booth, S. A. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-01999-w · Cited by 2 · see citing works
Self-citationHuman Genetic Evidence for New Targets in Prion Diseases: Opportunities and Challenges
Hill, E., & Mead, S. (2025) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-3-031-97055-9_10 · Cited by 1 · see citing works
PrP C -induced signaling in human neurons activates phospholipase Cɣ1 and an Arc/Arg3.1 responsePreprint
Ojeda-Juárez, D., Funk, G., Richards, E., Rajic, A. J., McClatchy, D. B., Soldau, K., Chen, X., Yates, J. R., Gonias, S. L., & Sigurdson, C. J. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.01.645054 · Cited by 1 · see citing works
Zafar, S., Younas, N., Douet, J., Schmitz, M., Candelise, N., Correia, S., Andréoletti, O., & Zerr, I. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.17.676758 · Cited by 1 · see citing works
Slota, J. A., Sajesh, B. V., Frost, K. F., Medina, S. J., & Booth, S. A. (2022) · Figshare · doi:10.6084/m9.figshare.21532645
Self-citationOjeda-Juárez, D., Funk, G., McClatchy, D. B., Richards, E., Rajic, A. J., Soldau, K., Geschwind, M. D., Chen, X., Yates, J. R., Gonias, S. L., et al. (2026) · Stem Cell Reports · doi:10.1016/j.stemcr.2026.102924 · Cited by 1 · see citing works
- Authors
- Slota, J. A., Medina, S. J., Frost, K. L., & Booth, S. A.
- Affiliations
- Public Health Agency of Canada (CA)
- Corresponding author
- Booth, Stephanie A.
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2022-05-16
- Volume
- 16
- Pages
- 918811-918811
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC9149297
- OpenAlex
- W4280558165
- Cited by
- 16
- References
- 98
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 3 · 2023: 1 · 2022: 4
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Public Health Agency of Canada
- Public Health Agency
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- prion disease, gene expression profiling, hippocampal CA1, thalamus, astrocytes, microglia, reactive microglia, synaptic dysfunction, neurodegeneration, brain cell types, preclinical disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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