Evidence map›Paper›PMID 21381115›Full record

ArticleGlia2011

Loss of adenomatous polyposis coli in Bergmann glia disrupts their unique architecture and leads to cell nonautonomous neurodegeneration of cerebellar Purkinje neurons.

Xiaohong Wang, Tetsuya Imura, Michael V Sofroniew, Shinji Fushiki

Open access · greenAbstract read
In one paragraph

Article in Glia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. APC in the nervous system.Medical molecular morphology · 2026
    Review
  2. Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Review
  4. Article
  5. Uncovering cilia function in glial development.Annals of human genetics · 2024
    Review
  6. 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 · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. N-cadherin provides aProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Article
  14. Embryology.Handbook of clinical neurology · 2018
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Xiaohong WangDepartment of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tetsuya Imura
Michael V Sofroniew
Shinji Fushiki
Kyoto Prefectural University of Medicine · JPUniversity of California, Los Angeles · US

Funding

Molecular Dissection of Reactive Astrogliosis: STAT3R01NS057624 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SOFRONIEW, MICHAEL V · 2008 to 2012
$1.8M
NINDS NIH HHS NS057624NINDS NIH HHS R01 NS057624
6 · The paper itself

Abstract

The tumor suppressor adenomatous polyposis coli (APC) is a multifunctional protein that inhibits the Wnt/beta-catenin signaling pathway and regulates the microtubule and actin cytoskeletons. Using conditional knockout (CKO) mice in which the APC gene is inactivated in glial fibrillary acidic protein (GFAP)-expressing cells, we show a selective and critical role for APC in maintaining the morphology and function of cerebellar Bergmann glia, which are specialized astroglia that extend polarized radial processes from the Purkinje cell layer to the pial surface. APC-CKO mice developed Bergmann glia normally until the accumulation of beta-catenin started around postnatal day 10 (P10). Their radial fibers then became shortened with a marked reduction of branching collaterals and their cell bodies translocated into the molecular layer followed by loss of their pial contact and transformation into stellate-shaped cells by P21. Purkinje neurons were normal in appearance and number at P21, but there was significant loss of Purkinje neurons and cerebellar atrophy by middle age. Outside the cerebellum, neither beta-catenin accumulation nor morphological changes were identified in GFAP-expressing astroglia, indicating region-specific effects of APC deletion and an essential role for APC in maintaining the unique morphology of Bergmann glia as compared with other astroglia. These results demonstrate that loss of APC selectively disrupts the Bergmann glial scaffold in late postnatal development and leads to cerebellar degeneration with loss of Purkinje neurons in adults, providing another potential mechanism for region-specific non-cell autonomous neurodegeneration.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsCerebellar DiseasesCerebellumDisease Models, AnimalGenetic Predisposition to DiseaseMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNerve DegenerationNeurogliaPurkinje CellsAdenomatous Polyposis Coli Protein

Identifiers

PMID21381115
PMCPMC3287075
OpenAlexW2007520287

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.