ArticleJournal of neuroinflammation2017
Inhibition of colony-stimulating factor 1 receptor early in disease ameliorates motor deficits in SCA1 mice.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Pharmacological Depletion of Retinal Mononuclear Phagocytes Is Neuroprotective in a Mouse Model of Mitochondrial Optic Neuropathy.Investigative ophthalmology & visual science · 2026Article
- Molecular hallmarks of neurodegeneration in polyglutamine spinocerebellar ataxias.Cell death & disease · 2025Review
- 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
- 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
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Long-term reprogramming of primed microglia after moderate inhibition of CSF1R signaling.Glia · 2025Article
- The Neuroimmune System and the Cerebellum.Cerebellum (London, England) · 2024Review
- 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
- Therapeutic Strategies for Spinocerebellar Ataxia Type 1.Biomolecules · 2023Review
- 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
- BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1.Neurobiology of disease · 2023Article
- Deletion of Small GTPase H-Ras Rescues Memory Deficits and Reduces Amyloid Plaque-Associated Dendritic Spine Loss in Transgenic Alzheimer's Mice.Molecular neurobiology · 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
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Spatial and Temporal Diversity of Astrocyte Phenotypes in Spinocerebellar Ataxia Type 1 Mice.Cells · 2022Article
- Leukocyte Telomere Length Variability as a Potential Biomarker in Patients with PolyQ Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- Microglial Depletion Has No Impact on Disease Progression in a Mouse Model of Machado-Joseph Disease.Cells · 2022Article
- Consensus Paper: Strengths and Weaknesses of Animal Models of Spinocerebellar Ataxias and Their Clinical Implications.Cerebellum (London, England) · 2022Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPolyglutamine (polyQ) expansion in the protein Ataxin-1 (ATXN1) causes spinocerebellar ataxia type 1 (SCA1), a fatal dominantly inherited neurodegenerative disease characterized by motor deficits, cerebellar neurodegeneration, and gliosis. Currently, there are no treatments available to delay or ameliorate SCA1. We have examined the effect of depleting microglia during the early stage of disease by using PLX, an inhibitor of colony-stimulating factor 1 receptor (CSFR1), on disease severity in a mouse model of SCA1.
methodsTransgenic mouse model of SCA1, ATXN1[82Q] mice, and wild-type littermate controls were treated with PLX from 3 weeks of age. The effects of PLX on microglial density, astrogliosis, motor behavior, atrophy, and gene expression of Purkinje neurons were examined at 3 months of age.
resultsPLX treatment resulted in the elimination of 70-80% of microglia from the cerebellum of both wild-type and ATXN1[82Q] mice. Importantly, PLX ameliorated motor deficits in SCA1 mice. While we have not observed significant improvement in the atrophy or disease-associated gene expression changes in Purkinje neurons upon PLX treatment, we have detected reduced expression of pro-inflammatory cytokine tumor necrosis factor alpha (TNFα) and increase in the protein levels of wild-type ataxin-1 and post-synaptic density protein 95 (PSD95) that may help improve PN function.
conclusionsA decrease in the number of microglia during an early stage of disease resulted in the amelioration of motor deficits in SCA1 mice.
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