ArticleGlia2018
Astroglia contribute to the pathogenesis of spinocerebellar ataxia Type 1 (SCA1) in a biphasic, stage-of-disease specific manner.
Article in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Immune Activation and Glial Dysfunction in Spinocerebellar Ataxias: From Cerebellar Landscape to Disease-Driven Mechanisms and Immunomodulation.Cerebellum (London, England) · 2026Review
- 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
- Transcriptomic and Proteomic Changes in the Brain Along with Increasing Phenotypic Severity in a Rat Model of Neonatal Hyperbilirubinemia.International journal of molecular sciences · 2025Article
- Fingolimod Prevents Neuroinflammation but Has a Limited Effect on the Development of Ataxia in a Mouse Model for SCA1.International journal of molecular sciences · 2025Article
- Sex Differences in a Novel Mouse Model of Spinocerebellar Ataxia Type 1 (SCA1).International journal of molecular sciences · 2025Article
- Astroglial modulation of synaptic function in the non-demyelinated cerebellar cortex is dependent on MyD88 signaling in a model of toxic demyelination.Journal of neuroinflammation · 2025Article
- Dietary and lifestyle interventions for the management of hereditary ataxias.Frontiers in nutrition · 2025Review
- Article
- Cerebellar Heterogeneity and Selective vulnerability in Spinocerebellar Ataxia Type 1 (SCA1).Neurobiology of disease · 2024Article
- Longitudinal single-cell transcriptional dynamics throughout neurodegeneration in SCA1.Neuron · 2024Article
- Altered calcium signaling in Bergmann glia contributes to spinocerebellar ataxia type-1 in a mouse model of SCA1.Neurobiology of disease · 2023Article
- Reactive Bergmann glia play a central role in spinocerebellar ataxia inflammation via the JNK pathway.Journal of neuroinflammation · 2023Article
- BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1.Neurobiology of disease · 2023Article
- Modest Reduction in CAG Repeat Length Rescues Motor Deficits but Not Purkinje Cell Pathology and Gliosis in Spinocerebellar Ataxia Type 1 Mice.Neuroglia (Basel, Switzerland) · 2023Article
- Contribution of Glial Cells to Polyglutamine Diseases: Observations from Patients and Mouse Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Spatial and Temporal Diversity of Astrocyte Phenotypes in Spinocerebellar Ataxia Type 1 Mice.Cells · 2022Article
- Differential effects of Wnt-β-catenin signaling in Purkinje cells and Bergmann glia in spinocerebellar ataxia type 1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of the ataxin-1 interaction network and its impact on spinocerebellar ataxia type 1.Human genomics · 2022Article
- Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications.Cerebellum (London, England) · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene. SCA1 is characterized by balance and coordination deficits due to the predominant loss of Purkinje neurons in the cerebellum. We previously demonstrated that cerebellar astrogliosis beings during the early stages of SCA1, prior to onset of motor deficits and loss of Purkinje neurons. We communicate here that cerebellar astrogliosis contributes to SCA1 pathogenesis in a biphasic, stage of disease dependent manner. We modulated astrogliosis by selectively reducing pro-inflammatory transcriptional regulator nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling in astroglia via a Cre-lox mouse genetic approach. Our results indicate that inhibition of astroglial NF-κB signaling, prior to motor deficit onset, exacerbates disease severity. This is suggestive of a neuroprotective role mediated by astroglia during early stage SCA1. In contrast, inhibition of astroglial NF-κB signaling during late stage of disease ameliorated motor deficits, indicating a potentially harmful role of astroglia late in SCA1. These results indicate that astrogliosis may have a critical and dual role in disease. If so, our results imply that anti-inflammatory astroglia-based therapeutic approaches may need to consider disease progression to achieve therapeutic efficacy.
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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.