ArticlePrion2018
Altered gene transcription linked to astrocytes and oligodendrocytes in frontal cortex in Creutzfeldt-Jakob disease.
Article in Prion, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Distinct neuronal alterations distinguish two subtypes of sporadic Creutzfeldt-Jakob disease with shared dysfunctional pathways.The Journal of clinical investigation · 2026Article
- Alterations in cerebrospinal fluid levels of myelin- and oligodendrocyte-related proteins in sporadic Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2026Article
- Multiomic analyses direct hypotheses for Creutzfeldt-Jakob disease risk genes.Brain : a journal of neurology · 2025Article
- SEE: A Method for Predicting the Dynamics of Chromatin Conformation Based on Single-Cell Gene Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Correlation between blood biomarkers and post-stroke cognitive impairment.Frontiers in aging neuroscience · 2025Article
- A Systematic Review of Sporadic Creutzfeldt-Jakob Disease: Pathogenesis, Diagnosis, and Therapeutic Attempts.Neurology international · 2024Review
- Tau, Glial Fibrillary Acidic Protein, and Neurofilament Light Chain as Brain Protein Biomarkers in Cerebrospinal Fluid and Blood for Diagnosis of Neurobiological Diseases.International journal of molecular sciences · 2024Review
- Oligodendrocyte-derived transcellular signaling regulates axonal energy metabolism.Current opinion in neurobiology · 2023Review
- Article
- Genomic, transcriptomic and RNA editing analysis of human MM1 and VV2 sporadic Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2022Article
- Neuroprotection and neuroregeneration: roles for the white matter.Neural regeneration research · 2022Review
- Differential astrocyte and oligodendrocyte vulnerability in murine Creutzfeldt-Jakob disease.Prion · 2021Article
- Histotype-Dependent Oligodendroglial PrP Pathology in Sporadic CJD: A Frequent Feature of the M2C "Strain".Viruses · 2021Article
- Oligodendroglial Energy Metabolism and (re)Myelination.Life (Basel, Switzerland) · 2021Review
- Altered mRNA and Protein Expression of Monocarboxylate Transporter MCT1 in the Cerebral Cortex and Cerebellum of Prion Protein Knockout Mice.International journal of molecular sciences · 2021Article
- MCT1 Deletion in Oligodendrocyte Lineage Cells Causes Late-Onset Hypomyelination and Axonal Degeneration.Cell reports · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted expression of genes coding for proteins specific to astrocytes, oligodendrocytes and myelin was performed in frontal cortex area 8 of Creutzfeldt-Jakob disease methionine/methionine and valine/valine (CJD MM1 and VV2, respectively) compared with controls. GFAP (glial fibrillary acidic protein) mRNA was up-regulated whereas SLC1A2 (solute carrier family 1 member 2, coding for glutamate transporter 1: GLT1), AQ4 (aquaporin 4), MPC1 (mitochondrial pyruvate carrier 1) and UCP5 (mitochondrial uncoupled protein 5) mRNAs were significantly down-regulated in CJD MM1 and CJD VV2, and GJA1 (connexin 43) in CJD VV2. OLIG1 and OLIG2 (oligodendocyte transcription factor 1 and 2, respectively), SOX10 (SRY-Box10) and oligodendroglial precursor cell (OPC) marker NG2 (neuronal/glial antigen) 2 were preserved, but GALC (coding for galactosylceramidase), SLC2A1 (solute carrier family 2 member 1: glucose transporter member 1: GLUT1) and MCT1 (monocarboxylic acid transporter 1) mRNA expression levels were significantly reduced in CJD MM1 and CJD VV2. Expression levels of most genes linked to myelin were not altered in the cerebral cortex in CJD. Immunohistochemistry to selected proteins disclosed individual variations but GFAP, Olig-2, AQ4 and GLUT1 correlated with mRNA levels, whereas GLT1 was subjected to individual variations. However, MPC1, UCP5 and MCT1 decrease was more closely related to the respective reduced neuronal immunostaining. These observations support the idea that molecular deficits linked to energy metabolism and solute transport in astrocytes and oligodendrocytes, in addition to neurons, are relevant in the pathogenesis of cortical lesions in CJD.
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