Evidence map›Paper›PMID 30152044›Full record

ArticleGlia2018

Astrocytes and neurons produce distinct types of polyglucosan bodies in Lafora disease.

Elisabet Augé, Carme Pelegrí, Gemma Manich, Itsaso Cabezón, Joan J Guinovart, Jordi Duran, Jordi Vilaplana

Open access · greenAbstract readComparative Study
In one paragraph

Article in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Article
  6. Article
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  11. Polyglucosan body disease in an aged chimpanzee (Pan troglodytes).Neuropathology : official journal of the Japanese Society of Neuropathology · 2023
    Article
  12. Article
  13. Review
  14. Uncovering tau in wasteosomes (Frontiers in aging neuroscience · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Wasteosomes (Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

7 authors at 3 institutions in 1 country.

Elisabet AugéSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Barcelona, Spain.
Carme PelegríSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Barcelona, Spain.
Gemma ManichSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Barcelona, Spain.
Itsaso CabezónSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Barcelona, Spain.
Joan J GuinovartInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Jordi DuranInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Jordi VilaplanaSecció de Fisiologia, Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Barcelona, Spain.
Universitat de Barcelona · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ES

Funding

Suppressing glycogen storage with small molecule inhibitors as a therapeutic approach to Lafora DiseaseP01NS097197 · NINDS · UNIVERSITY OF KENTUCKY · PI GAO, TIANYAN · 2016 to 2021
$9.0M
NINDS NIH HHS P01 NS097197NINDS NIH HHS P01NS097197
6 · The paper itself

Abstract

Lafora disease (LD), the most devastating adolescence-onset epilepsy, is caused by mutations in the EPM2A or EPM2B genes, which encode the proteins laforin and malin, respectively. Loss of function of one of these proteins, which are involved in the regulation of glycogen synthesis, induces the accumulation of polyglucosan bodies (PGBs)-known as Lafora bodies (LBs) and associated with neurons-in the brain. Ageing and some neurodegenerative conditions lead to the appearance of another type of PGB called corpora amylacea, which are associated with astrocytes and contain neo-epitopes that can be recognized by natural antibodies. Here we studied the PGBs in the cerebral cortex and hippocampus of malin knockout mice, a mouse model of LD. These animals presented not only LBs associated with neurons but also a significant number of PGBs associated with astrocytes. These astrocytic PGBs were also increased in mice from senescence-accelerated mouse-prone 8 (SAMP8) strain and mice with overexpression of Protein Targeting to Glycogen (PTG

Indexed as

AnimalsAstrocytesCerebral CortexDisease Models, AnimalGlucansHippocampusInclusion BodiesLafora DiseaseMice, TransgenicNeuronsGlucanspolyglucosancorpora amylaceaLafora bodymalinnatural antibodyneo-epitope

Identifiers

PMID30152044
PMCPMC6240358
OpenAlexW2888918396

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.