ArticleMolecular neurobiology2014
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).
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Distinct neuronal alterations distinguish two subtypes of sporadic Creutzfeldt-Jakob disease with shared dysfunctional pathways.The Journal of clinical investigation · 2026Article
- High Proportions of GAP43 Positivity in the Cerebrospinal Fluids of Patients with Sporadic and Certain Types of Genetic Creutzfeldt-Jakob Diseases by Western Blot Analysis.International journal of molecular sciences · 2026Article
- Aberrance of GAP43/p-GAP43 Closely Associates with the Pathology of Neuron Loss in Prion-Infected Rodent Models.Molecular neurobiology · 2025Article
- Extensive Disturbances of Intracellular Components and Dysfunctions of Biological Pathways in the Brain Tissues During Prion Infection - China's Studies.China CDC weekly · 2022Review
- Identification of molecular signatures associated with sleep disorder and Alzheimer's disease.Frontiers in psychiatry · 2022Article
- The Three Glycotypes in the London Classification System of Sporadic Creutzfeldt-Jakob Disease Differ in Disease Duration.Molecular neurobiology · 2021Article
- Integrative genomics analysis identifies five promising genes implicated in insomnia risk based on multiple omics datasets.Bioscience reports · 2020Article
- RNA editing alterations define manifestation of prion diseases.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Sequence Alterations of Cortical Genes Linked to Individual Connectivity of the Human Brain.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Neuronal calcineurin transcriptional targets parallel changes observed in Alzheimer disease brain.Journal of neurochemistry · 2018Article
- Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases.Molecular neurobiology · 2016Article
- Biomarkers for sporadic Creutzfeldt-Jakob disease.Annals of clinical and translational neurology · 2016Review
- Insight into the Molecular Imaging of Alzheimer's Disease.International journal of biomedical imaging · 2016Review
- Proteomics analyses for the global proteins in the brain tissues of different human prion diseases.Molecular & cellular proteomics : MCP · 2015Article
- Strategies of Functional Foods Promote Sleep in Human Being.Current signal transduction therapy · 2014Article
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12 authors.
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Abstract
Neurodegenerative disease is a general designation for the disorders that are progressive loss of structure or function and final death of neurons, including Alzheimer's, Parkinson's, Huntington's, prion diseases, etc. In this study, we comparatively analyzed 21 individual microarray data sets of the cortex tissues from 11 sporadic Creutzfeldt-Jakob disease (sCJD), 3 fatal familial insomnia (FFI), 3 Alzheimer's disease (AD), and 4 normal controls. After normalization, a collection of 730 differently expressed sets (DESets) were obtained by comparison of the data of three diseases with their original controls. Principal component analysis (PCA) showed a background-related distribution within the groups of FFI, AD, and normal control, but two apparently different subgroups within the group of sCJD were observed. Review of the clinical materials of 11 sCJD patients identified the difference in brain PrP(Sc) deposits between two subgroups. Hierarchical cluster analysis illustrated the relatively independent clusters of normal controls, FFIs, six sCJD cases (subgroup 1) with more PrP(Sc) deposits, respectively, while an overlapped cluster of five cases of sCJD2 (subgroup 2) with less PrP(Sc) deposits and AD patients. Despite of the presence of special gene expressions, many common features were found among those neurodegenerative diseases. The most commonly changed biological processes (BPs) were signal transduction, synaptic transmission, and neuropeptide signaling pathway. The most commonly changed pathways were MAPK signaling pathway, Parkinson's disease, and oxidative phosphorylation. Our data here provide the similarity and difference in global gene expressions among the patients with sCJD, FFI, and AD, which may help to understand the common mechanism of neurodegenerative diseases.
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