ArticleNeuroscience2015
Early activation of microglia and astrocytes in mouse models of spinocerebellar ataxia type 1.
Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 113 citations in OpenAlex.
- Neuroprotection Across Cerebellar and Nigrostriatal Degeneration: Translational Insights from Parkinson's Disease to Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Review
- Immune Activation and Glial Dysfunction in Spinocerebellar Ataxias: From Cerebellar Landscape to Disease-Driven Mechanisms and Immunomodulation.Cerebellum (London, England) · 2026Review
- Review
- Long term administration of selective NMDA GluN2B receptor blocker Ro25-6981 attenuates neurodegeneration in mouse model of spinocerebellar ataxia type 1 (SCA1).Cell death discovery · 2026Article
- Translational Relevance of SCA1 Models for the Development of Therapies for Spinocerebellar Ataxia Type 1.Biomedicines · 2025Review
- Oral KDS2010, a Monoamine Oxidase-B (MAO-B) Inhibitor, Slows the Deterioration of Motor Coordination in Genetic SCA1 Models by Inhibiting Astrocytic MAO-B-Mediated Inflammation.Journal of neurochemistry · 2025Article
- Molecular hallmarks of neurodegeneration in polyglutamine spinocerebellar ataxias.Cell death & disease · 2025Review
- Roots of Progress: Uncovering Cerebellar Ataxias Using iPSC Models.Biomedicines · 2025Review
- A novel early onset spinocerebellar ataxia 13 BAC mouse model with cerebellar atrophy, tremor, and ataxic gait.Experimental animals · 2025Article
- An expanded polyglutamine in ATAXIN1 results in a loss-of-function that exacerbates severity of Multiple Sclerosis in an EAE mouse model.Journal of neuroinflammation · 2025Article
- Sex Differences in a Novel Mouse Model of Spinocerebellar Ataxia Type 1 (SCA1).International journal of molecular sciences · 2025Article
- A dominant negative Kcnd3 F227del mutation in mice causes spinocerebellar ataxia type 22 (SCA22) by impairing ER and Golgi functioning.The Journal of pathology · 2025Article
- The Neuroimmune System and the Cerebellum.Cerebellum (London, England) · 2024Review
- Post-symptomatic administration of hMSCs exerts therapeutic effects in SCA2 mice.Stem cell research & therapy · 2024Article
- Astrocyte-Mediated Neuroinflammation in Neurological Conditions.Biomolecules · 2024Review
- Article
- Altered lipid homeostasis is associated with cerebellar neurodegeneration in SNX14 deficiency.JCI insight · 2024Article
- Dynamic molecular network analysis of iPSC-Purkinje cells differentiation delineates roles of ISG15 in SCA1 at the earliest stage.Communications biology · 2024Article
- Longitudinal single-cell transcriptional dynamics throughout neurodegeneration in SCA1.Neuron · 2024Article
- Early molecular layer interneuron hyperactivity triggers Purkinje neuron degeneration in SCA1.Neuron · 2023Article
14 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 1 (SCA1) is an incurable, dominantly inherited neurodegenerative disease of the cerebellum caused by a polyglutamine-repeat expansion in the protein ataxin-1 (ATXN1). While analysis of human autopsy material indicates significant glial pathology in SCA1, previous research has focused on characterizing neuronal dysfunction. In this study, we characterized astrocytic and microglial response in SCA1 using a comprehensive array of mouse models. We have discovered that astrocytes and microglia are activated very early in SCA1 pathogenesis even when mutant ATXN1 expression was limited to Purkinje neurons. Glial activation occurred in the absence of neuronal death, suggesting that glial activation results from signals emanating from dysfunctional neurons. Finally, in all different models examined glial activation closely correlated with disease progression, supporting the development of glial-based biomarkers to follow disease progression.
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What OpenQuestion holds
Registered trials
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.