Email updates

Keep up to date with the latest news and content from BMC Genomics and BioMed Central.

Open Access Research article

Gene expression profiling of brains from bovine spongiform encephalopathy (BSE)-infected cynomolgus macaques

Maura Barbisin1, Silvia Vanni1, Ann-Christin Schmädicke2, Judith Montag24, Dirk Motzkus2, Lennart Opitz3, Gabriela Salinas-Riester3 and Giuseppe Legname1*

  • * Corresponding author: Giuseppe Legname

  • † Equal contributors

Author Affiliations

1 Department of Neuroscience, Scuola Internazionale Superiore di Studi Avanzati (SISSA), Via Bonomea 265, 34136 Trieste, Italy

2 Unit of Infection Models, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany

3 Microarray Core Facility, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077 Göttingen, Germany

4 Molecular and Cell Physiology, Hannover Medical School, Carl-Neuberg Str. 1, D-30625 Hannover, Germany

For all author emails, please log on.

BMC Genomics 2014, 15:434  doi:10.1186/1471-2164-15-434

Published: 5 June 2014



Prion diseases are fatal neurodegenerative disorders whose pathogenesis mechanisms are not fully understood. In this context, the analysis of gene expression alterations occurring in prion-infected animals represents a powerful tool that may contribute to unravel the molecular basis of prion diseases and therefore discover novel potential targets for diagnosis and therapeutics. Here we present the first large-scale transcriptional profiling of brains from BSE-infected cynomolgus macaques, which are an excellent model for human prion disorders.


The study was conducted using the GeneChip® Rhesus Macaque Genome Array and revealed 300 transcripts with expression changes greater than twofold. Among these, the bioinformatics analysis identified 86 genes with known functions, most of which are involved in cellular development, cell death and survival, lipid homeostasis, and acute phase response signaling. RT-qPCR was performed on selected gene transcripts in order to validate the differential expression in infected animals versus controls. The results obtained with the microarray technology were confirmed and a gene signature was identified. In brief, HBB and HBA2 were down-regulated in infected macaques, whereas TTR, APOC1 and SERPINA3 were up-regulated.


Some genes involved in oxygen or lipid transport and in innate immunity were found to be dysregulated in prion infected macaques. These genes are known to be involved in other neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. Our results may facilitate the identification of potential disease biomarkers for many neurodegenerative diseases.

Prion diseases; BSE; Non-human primates; Neurodegeneration; Transcriptome; Microarray; RT-qPCR; Biomarker; Serpina3; Hemoglobin