ArticleJournal of neurological sciences (Turkish)2006
Glial S100B Positive Vacuoles In Purkinje Cells: Earliest Morphological Abnormality In SCA1 Transgenic Mice.
Article in Journal of neurological sciences (Turkish), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Cerebellar Astrocytes: Much More Than Passive Bystanders In Ataxia Pathophysiology.Journal of clinical medicine · 2020Review
- Extracellular S100β Disrupts Bergman Glia Morphology and Synaptic Transmission in Cerebellar Purkinje Cells.Brain sciences · 2019Article
- Abnormalities in synaptic dynamics during development in a mouse model of spinocerebellar ataxia type 1.Scientific reports · 2015Article
- Focused cerebellar laser light induced hyperthermia improves symptoms and pathology of polyglutamine disease SCA1 in a mouse model.Cerebellum (London, England) · 2014Article
- Knockdown of acid-sensing ion channel 1a (ASIC1a) suppresses disease phenotype in SCA1 mouse model.Cerebellum (London, England) · 2014Article
- Suppression of calbindin-D28k expression exacerbates SCA1 phenotype in a disease mouse model.Cerebellum (London, England) · 2012Article
- The design and delivery of a thermally responsive peptide to inhibit S100B-mediated neurodegeneration.Neuroscience · 2011Article
- Glial S100B protein modulates mutant ataxin-1 aggregation and toxicity: TRTK12 peptide, a potential candidate for SCA1 therapy.Cerebellum (London, England) · 2011Article
- Cellular fusion for gene delivery to SCA1 affected Purkinje neurons.Molecular and cellular neurosciences · 2011Article
- Dopamine D2 receptor signaling modulates mutant ataxin-1 S776 phosphorylation and aggregation.Journal of neurochemistry · 2010Article
- Bergmann glial S100B activates myo-inositol monophosphatase 1 and Co-localizes to purkinje cell vacuoles in SCA1 transgenic mice.Cerebellum (London, England) · 2009Article
- Glial response to polyglutamine-mediated stress.Bioscience hypotheses · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia-1 (SCA1) is caused by the expansion of a polyglutamine repeat within the disease protein, ataxin-1. The overexpression of mutant ataxin-1 in SCA1 transgenic mice results in the formation of cytoplasmic vacuoles in Purkinje neurons (PKN) of the cerebellum. PKN are closely associated with neighboring Bergmann glia. To elucidate the role of Bergmann glia in SCA1 pathogenesis, cerebellar tissue from 7 days to 6 wks old SCA1 transgenic and wildtype mice were used. We observed that Bergmann glial S100B protein is localized to the cytoplasmic vacuoles in SCA1 PKN. These S100B positive cytoplasmic vacuoles began appearing much before the onset of behavioral abnormalities, and were negative for other glial and PKN marker proteins. Electron micrographs revealed that vacuoles have a double membrane. In the vacuoles, S100B colocalized with receptors of advanced glycation end-products (RAGE), and S100B co-immunoprecipated with cerebellar RAGE. In SCA1 PKN cultures, exogenous S100B protein interacted with the PKN membranes and was internalized. These data suggest that glial S100B though extrinsic to PKN is sequestered into cytoplasmic vacuoles in SCA1 mice at early postnatal ages. Further, S100B may be binding to RAGE on Purkinje cell membranes before these membranes are internalized.
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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.