Evidence map›Paper›PMID 9804383›Full record

ReviewBrain pathology (Zurich, Switzerland)1998

Mouse models of myelin diseases.

H Werner, M Jung, M Klugmann, M Sereda, I R Griffiths, K A Nave

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Misalignment of PLP/DM20 transmembrane domains determines protein misfolding in Pelizaeus-Merzbacher disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  8. Article
  9. Article
  10. Proteolipid protein is required for transport of sirtuin 2 into CNS myelin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  11. Article
  12. Myelinogenesis and axonal recognition by oligodendrocytes in brain are uncoupled in Olig1-null mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
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

6 authors at 2 institutions in 2 countries.

H WernerZentrum für Molekulare Biologie (ZMBH), Universität Heidelberg, Germany.
M Jung
M Klugmann
M Sereda
I R Griffiths
K A Nave
Heidelberg University · DEUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dys- and demyelination are the common endpoints of several inherited diseases of glial cells, which elaborate myelin and which maintain the myelin sheath very much like an "external" cellular organelle. Whereas some of the genes that are affected by mutations appear to be glial-specific, other genes are expressed in many cell types but their defect is restricted to oligodendrocytes or Schwann cells. Many of the disease genes and their encoded proteins have been studied with the help of mouse models, and a number of different molecular pathomechanisms have emerged which have been summarized in Figure 8. Some of the new concepts in the field, which have been addressed in this review, have only emerged because similar pathomechanisms were discovered for different myelin proteins. Mouse models have clearly helped to address both, the molecular pathology of myelin diseases and the normal function of myelin genes, but as discussed in this review, these questions turned out to be very different. Despite the progress in understanding the role of the abundant myelin proteins, there also remain a number of open questions that concern, among other things, the initial axon-glia recognition, the assembly process of the myelin sheath, and the long-term interaction of axons with their myelinating glia. Finally, animal models of human neurological diseases should not be restricted to the study of pathology, but they should also contribute to the development of experimental treatments. It is encouraging that a few attempts have been made.

Indexed as

AnimalsDemyelinating DiseasesHumansMiceMice, TransgenicMutationMyelin Sheath

Identifiers

PMID9804383
PMCPMC8098187
OpenAlexW2002871398

What OpenQuestion holds

Textmetadata
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.