ArticleGlia2017
Frequency of nuclear mutant huntingtin inclusion formation in neurons and glia is cell-type-specific.
Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 115 citations in OpenAlex.
- Huntington's disease vasculopathy is barrier-type-selective and arteriolar-dominant with spatially-coupled astrogliosis and reversible by S1pr1 stimulation.Nature communications · 2026Article
- L-theanine from Camellia sinensis (L.) attenuates 3-NP-induced Huntington's disease-like alterations by remedying behavioral patterns and modulating neurotransmitters across three distinct brain regions: evidence from in-vivo and in-silico approaches.Metabolic brain disease · 2026Article
- Astrocyte heterogeneity and gliosis in Huntington's disease: Histopathological insights into striatal and white matter pathology.Histology and histopathology · 2026Review
- Astrocytic noncanonical WNT5B signaling modulates extracellular matrix remodeling and neuropathology in Huntington's disease.Signal transduction and targeted therapy · 2026Article
- Differential effects of overexpression of mutant huntingtin and TDP-43 in agouti-related protein neurons in the arcuate nucleus of the hypothalamus in mice.Acta neuropathologica communications · 2025Article
- Astrocyte-neuron combined targeting for CYP46A1 gene therapy in Huntington's disease.Acta neuropathologica communications · 2025Article
- Article
- Targeting IDO1 in Huntington's Disease: Network Pharmacology and Preclinical Evidence from Coffea arabica.Neurochemical research · 2025Article
- Microglial immune memory in Parkinson's and Huntington's diseases: epigenetics, triggers, and therapies.Epigenomics · 2025Review
- Glial phagocytosis for synapse and toxic proteins in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Progress in AAV-Mediated In Vivo Gene Therapy and Its Applications in Central Nervous System Diseases.International journal of molecular sciences · 2025Review
- Mapping the glial transcriptome in Huntington's disease using snRNAseq: selective disruption of glial signatures across brain regions.Acta neuropathologica communications · 2024Article
- Evolution of aberrant brain-wide spatiotemporal dynamics of resting-state networks in a Huntington's disease mouse model.Clinical and translational medicine · 2024Article
- Astrocyte morphology.Trends in cell biology · 2024Review
- Review
- Immunological aspects of central neurodegeneration.Cell discovery · 2024Review
- 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
- Copper enhances aggregational toxicity of mutant huntingtin in a Drosophila model of Huntington's Disease.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Beneficial effects of miR-132/212 deficiency in the zQ175 mouse model of Huntington's disease.Frontiers in neuroscience · 2024Article
- The phase coherence of the neurovascular unit is reduced in Huntington's disease.Brain communications · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disorder that is caused by a CAG expansion in the Huntingtin (HTT) gene, leading to HTT inclusion formation in the brain. The mutant huntingtin protein (mHTT) is ubiquitously expressed and therefore nuclear inclusions could be present in all brain cells. The effects of nuclear inclusion formation have been mainly studied in neurons, while the effect on glia has been comparatively disregarded. Astrocytes, microglia, and oligodendrocytes are glial cells that are essential for normal brain function and are implicated in several neurological diseases. Here we examined the number of nuclear mHTT inclusions in both neurons and various types of glia in the two brain areas that are the most affected in HD, frontal cortex, and striatum. We compared nuclear mHTT inclusion body formation in three HD mouse models that express either full-length HTT or an N-terminal exon1 fragment of mHTT, and we observed nuclear inclusions in neurons, astrocytes, oligodendrocytes, and microglia. When studying the frequency of cells with nuclear inclusions in mice, we found that half of the population of neurons contained nuclear inclusions at the disease end stage, whereas the proportion of GFAP-positive astrocytes and oligodendrocytes having a nuclear inclusion was much lower, while microglia hardly showed any nuclear inclusions. Nuclear inclusions were also present in neurons and all studied glial cell types in human patient material. This is the first report to compare nuclear mHTT inclusions in glia and neurons in different HD mouse models and HD patient brains. GLIA 2016;65:50-61.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.