ArticleMolecular neurobiology2013
Comparative analysis of gene expression profiles between cortex and thalamus in Chinese fatal familial insomnia patients.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Altered energy metabolism in Fatal Familial Insomnia cerebral organoids is associated with astrogliosis and neuronal dysfunction.PLoS genetics · 2023Article
- Extensive Disturbances of Intracellular Components and Dysfunctions of Biological Pathways in the Brain Tissues During Prion Infection - China's Studies.China CDC weekly · 2022Review
- Integrative genomics analysis identifies five promising genes implicated in insomnia risk based on multiple omics datasets.Bioscience reports · 2020Article
- Article
- Recent advances in the histo-molecular pathology of human prion disease.Brain pathology (Zurich, Switzerland) · 2019Review
- Comparison of village dog and wolf genomes highlights the role of the neural crest in dog domestication.BMC biology · 2018Article
- Fatal Familial Insomnia: Clinical Aspects and Molecular Alterations.Current neurology and neuroscience reports · 2017Review
- Fatal familial insomnia: mitochondrial and protein synthesis machinery decline in the mediodorsal thalamus.Brain pathology (Zurich, Switzerland) · 2017Article
- Gene markers of fracture healing in early stage and the regulatory mechanism during the process using microarray analysis.Acta orthopaedica et traumatologica turcica · 2016Article
- Distribution of Misfolded Prion Protein Seeding Activity Alone Does Not Predict Regions of Neurodegeneration.PLoS biology · 2016Article
- Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases.Molecular neurobiology · 2016Article
- Activation of the AMPK-ULK1 pathway plays an important role in autophagy during prion infection.Scientific reports · 2015Article
- Proteomics analyses for the global proteins in the brain tissues of different human prion diseases.Molecular & cellular proteomics : MCP · 2015Article
- Article
- Apparent reduction of ADAM10 in scrapie-infected cultured cells and in the brains of scrapie-infected rodents.Molecular neurobiology · 2014Article
- Remarkable reductions of PAKs in the brain tissues of scrapie-infected rodent possibly linked closely with neuron loss.Medical microbiology and immunology · 2014Review
- Analyses of the similarity and difference of global gene expression profiles in cortex regions of three neurodegenerative diseases: sporadic Creutzfeldt-Jakob disease (sCJD), fatal familial insomnia (FFI), and Alzheimer's disease (AD).Molecular neurobiology · 2014Article
- Global protein differential expression profiling of cerebrospinal fluid samples pooled from Chinese sporadic CJD and non-CJD patients.Molecular neurobiology · 2014Article
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatal familial insomnia (FFI) is a special subtype of genetic human prion diseases that is caused by the D178N mutation of the prion protein gene (PRNP). According to the surveillance data from 2006, FFI accounts for about half of all genetic prion disease cases in China. In this study, global expression patterns of the thalamus and parietal cortex from three patients with FFI were analyzed by Affymetrix Human Genome U133+ 2.0 chip. A total of 1,314 genes in the thalamus and 332 ones in the parietal lobe were determined to be differentially expressed genes (DEGs). The percentage of upregulated DEGs is much less in the thalamus (19.3 %) than that in the parietal lobe (42.8 %). Moreover, 255 of those DEGs showed the same altering tendencies in both tested regions, including 99 upregulated and 156 downregulated ones. The reliability of the results was confirmed by the real-time RT-PCR assays. There were 1,152 and 531 biological processes affected in the thalamus and the parietal lobe, respectively, as well as 391 overlapping ones in both regions. The most significantly changed molecular functions included transcription and DNA-dependent regulation of transcription, RNA splicing, mitochondrial electron transport, etc. The changed functions in the thalamus contained more numbers of DEGs than parietal lobe. According to KEGG classification, there were 167 and 115 different pathways changed in the thalamus and the parietal lobe, respectively, while 102 were changed in both. Interestingly, the top three changed pathways in the three groups mentioned above were Parkinson's disease, Alzheimer's disease, and oxidative phosphorylation. These results demonstrate the greater damage in the thalamus than in the parietal lobe during FFI pathogenesis, which is consistent with previous pathological observations. This study aims to describe the global expression profiles in various brain regions of FFI while proposing useful clues for understanding the pathogenesis of FFI and selecting potential biomarkers for diagnostic and therapeutic tools.
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