ArticleNeurochemical research2015
Trehalose attenuates the gait ataxia and gliosis of spinocerebellar ataxia type 17 mice.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Immune Activation and Glial Dysfunction in Spinocerebellar Ataxias: From Cerebellar Landscape to Disease-Driven Mechanisms and Immunomodulation.Cerebellum (London, England) · 2026Review
- Alimentary Treatment with Trehalose in a Pharmacological Model of Alzheimer's Disease in Mice: Effects of Different Dosages and Treatment Regimens.Pharmaceutics · 2024Article
- Progress in the discovery and development of small molecule methuosis inducers.RSC medicinal chemistry · 2023Review
- Profiling neuroprotective potential of trehalose in animal models of neurodegenerative diseases: a systematic review.Neural regeneration research · 2023Review
- Suppressing gain-of-function proteins via CRISPR/Cas9 system in SCA1 cells.Scientific reports · 2022Article
- Current and emerging treatment modalities for spinocerebellar ataxias.Expert review of neurotherapeutics · 2022Review
- New Perspectives of Gene Therapy on Polyglutamine Spinocerebellar Ataxias: From Molecular Targets to Novel Nanovectors.Pharmaceutics · 2021Review
- Trehalose in Machado-Joseph Disease: Safety, Tolerability, and Efficacy.Cerebellum (London, England) · 2020Article
- Targeting Inflammation, PHA-767491 Shows a Broad Spectrum in Protein Aggregation Diseases.Journal of molecular neuroscience : MN · 2020Article
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- Trehalose alleviates the phenotype of Machado-Joseph disease mouse models.Journal of translational medicine · 2020Article
- Lactulose and Melibiose Attenuate MPTP-Induced Parkinson's Disease in Mice by Inhibition of Oxidative Stress, Reduction of Neuroinflammation and Up-Regulation of Autophagy.Frontiers in aging neuroscience · 2020Article
- Genetics, Mechanisms, and Therapeutic Progress in Polyglutamine Spinocerebellar Ataxias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Chemical Screening Approaches Enabling Drug Discovery of Autophagy Modulators for Biomedical Applications in Human Diseases.Frontiers in cell and developmental biology · 2019Review
- Association Between Autophagy and Neurodegenerative Diseases.Frontiers in neuroscience · 2018Review
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Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinocerebellar ataxia type 17 (SCA17) is caused by CAG/CAA repeat expansion on the gene encoding a general transcription factor, TATA-box-binding protein (TBP). The CAG repeat expansion leads to the reduced solubility of polyglutamine TBP and induces aggregate formation. The TBP aggregation, mostly present in the cell nuclei, is distinct from that in most other neurodegenerative diseases, in which the aggregation is formed in cytosol or extracellular compartments. Trehalose is a disaccharide issued by the Food and Drug Administration with a Generally Recognized As Safe status. Lines of evidence suggest trehalose could prevent protein aggregate formation in several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. In this study, we evaluated the therapeutic potential of trehalose on SCA17 using cerebellar primary and organotypic culture systems and a mouse model. Our results showed that TBP nuclear aggregation was significantly decreased in both the primary and slice cultures. Trehalose (4 %) was further supplied in the drinking water of SCA17 transgenic mice. We found both the gait behavior in the footprint analysis and motor coordination in the rotarod task were significantly improved in the trehalose-treated SCA17 mice. The cerebellar weight was increased and the astrocyte gliosis was reduced in SCA17 mice after trehalose treatment. These data suggest that trehalose could be a potential nontoxic treatment for SCA17.
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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.