Gene expression profiling of scrapie-infected brain tissue

Riemer, Constanze; Neidhold, Sabine; Burwinkel, Michael; Schwarz, Anja; Schultz, Julia; Krätzschmar, Jörn; Mönning, Ursula; Baier, Michael

doi:10.1016/j.bbrc.2004.08.124

Cited by 109Prion Diseases and Protein MisfoldingAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Gene expression profiling of scrapie-infected brain tissue

Riemer, Constanze, Neidhold, Sabine, Burwinkel, Michael, Schwarz, Anja, Schultz, Julia, Krätzschmar, Jörn, Mönning, Ursula, Baier, Michael·2004·Biochemical and Biophysical Research Communications

DOI 10.1016/j.bbrc.2004.08.124

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Abstract

The underlying pathomechanisms in prion infections of the central nervous system are still insufficiently understood. The identification of genes with altered expression patterns in the diseased brain may provide insight into the disease development on the molecular level, which ultimately leads to neuronal loss. To provide a detailed analysis of changes in the molecular level in prion disease pathology we used a large-scale gene array based approach, which covers more than 11,000 functionally characterised sequences and expressed sequence tags, for the analysis of gene expression profile alterations in the cortex, medulla, and pons of scrapie-infected mice. The study identified in total 114 genes with altered mRNA levels, the majority of which were previously not known to be affected by the disease. Overall the gene array data demonstrate the presence of a strong inflammatory reaction and stress response, and show similarities to gene expression patterns found in brains affected by Alzheimer's disease and aging, respectively.

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Several proinflammatory cytokines, including TNF α, IL 1α, and C1qa, are upregulated in the brain during the prion disease course.
“Several proinflammatory cytokines are upregulated in the brain during the prion disease course including TNF α, IL 1α, and C1qa [46,69,70,71,72,73].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [69]

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Authors: Riemer, C., Neidhold, S., Burwinkel, M., Schwarz, A., Schultz, J., Krätzschmar, J., Mönning, U., & Baier, M.
Affiliations: Robert Koch Institute (DE)
Corresponding author: Baier, Michael
ORCID: Burwinkel, Michael
Schwarz, Anja
Baier, Michael
Venue: Biochemical and Biophysical Research Communications
Publisher: Elsevier BV
Published: 2004-10
Volume: 323
Issue: 2
Pages: 556-564
ISSN: 0006-291X (ISSN-L)
DOI: 10.1016/j.bbrc.2004.08.124
OpenAlex: W1966658105
Cited by: 108
References: 54
Citations by year: 2022: 4 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 5 · 2015: 5 · 2014: 7 · 2013: 4 · 2012: 8
FWCI: 2.61
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochemical and Biophysical Research Communications (publishedVersion)
PubMed (publishedVersion)
Funders: Bundesministerium für Bildung und Forschung
Bundesministerium für Gesundheit
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: scrapie, prion disease, gene expression profiling, brain transcriptome, neuroinflammation, stress response, neuronal loss, cerebral cortex, medulla, passive optical networks, Alzheimer's disease, aging, mouse model
MeSH terms: Animals, Brain, Encephalitis, Gene Expression Regulation, Mice, Inbred C57BL, Nerve Tissue Proteins, Scrapie, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Mice

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Gene expression profiling of scrapie-infected brain tissue

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