ArticleBMC medical genomics2014
A common gene expression signature in Huntington's disease patient brain regions.
Article in BMC medical genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Pooled it
- The HTT1a protein initiates HTT aggregation in a knock-in mouse model of Huntington's disease.Brain : a journal of neurology · 2026Article
- Cell-specific mechanisms drive connectivity across the time course of Huntington's disease.Nature communications · 2025Article
- Evaluating the neuroprotective potential ofIn silico pharmacology · 2025Article
- Identification of molecular targets and small drug candidates for Huntington's disease via bioinformatics and a network-based screening approach.Journal of cellular and molecular medicine · 2024Article
- CMS121 Partially Attenuates Disease Progression in Mouse Models of Huntington's Disease.Molecular neurobiology · 2024Article
- TYROBP/DAP12 knockout in Huntington's disease Q175 mice cell-autonomously decreases microglial expression of disease-associated genes and non-cell-autonomously mitigates astrogliosis and motor deterioration.Journal of neuroinflammation · 2024Article
- Genetic topography and cortical cell loss in Huntington's disease link development and neurodegeneration.Brain : a journal of neurology · 2023Article
- A Systematic Investigation of Complement and Coagulation-Related Protein in Autism Spectrum Disorder Using Multiple Reaction Monitoring Technology.Neuroscience bulletin · 2023Article
- Cerebellar granule neurons induce Cyclin D1 before the onset of motor symptoms in Huntington's disease mice.Acta neuropathologica communications · 2023Article
- A Comprehensive Bioinformatics Approach to Identify Molecular Signatures and Key Pathways for the Huntington Disease.Bioinformatics and biology insights · 2023Article
- Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis.International journal of molecular sciences · 2022Article
- Immortalized striatal precursor neurons from Huntington's disease patient-derived iPS cells as a platform for target identification and screening for experimental therapeutics.Human molecular genetics · 2021Article
- Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021Review
- Interleukin-6 deficiency exacerbates Huntington's disease model phenotypes.Molecular neurodegeneration · 2020Article
- Transcriptomic analysis of brain tissues identifies a role for CCAAT enhancer binding protein β in HIV-associated neurocognitive disorder.Journal of neuroinflammation · 2020Article
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Combination of stem cell and gene therapy ameliorates symptoms in Huntington's disease mice.NPJ Regenerative medicine · 2019Article
- Early alteration of epigenetic-related transcription in Huntington's disease mouse models.Scientific reports · 2018Article
- Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease.RNA biology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGene expression data provide invaluable insights into disease mechanisms. In Huntington's disease (HD), a neurodegenerative disease caused by a tri-nucleotide repeat expansion in the huntingtin gene, extensive transcriptional dysregulation has been reported. Conventional dysregulation analysis has shown that e.g. in the caudate nucleus of the post mortem HD brain the gene expression level of about a third of all genes was altered. Owing to this large number of dysregulated genes, the underlying relevance of expression changes is often lost in huge gene lists that are difficult to comprehend.
methodsTo alleviate this problem, we employed weighted correlation network analysis to archival gene expression datasets of HD post mortem brain regions.
resultsWe were able to uncover previously unidentified transcription dysregulation in the HD cerebellum that contained a gene expression signature in common with the caudate nucleus and the BA4 region of the frontal cortex. Furthermore, we found that yet unassociated pathways, e.g. global mRNA processing, were dysregulated in HD. We provide evidence to show that, contrary to previous findings, mutant huntingtin is sufficient to induce a subset of stress response genes in the cerebellum and frontal cortex BA4 region. The comparison of HD with other neurodegenerative disorders showed that the immune system, in particular the complement system, is generally activated. We also demonstrate that HD mouse models mimic some aspects of the disease very well, while others, e.g. the activation of the immune system are inadequately reflected.
conclusionOur analysis provides novel insights into the molecular pathogenesis in HD and identifies genes and pathways as potential therapeutic targets.
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