Evidence map›Paper›PMID 17498694›Full record

ReviewExperimental cell research2007

GFAP and its role in Alexander disease.

Roy A Quinlan, Michael Brenner, James E Goldman, Albee Messing

Open access · greenAbstract readReview
In one paragraph

Review in Experimental cell research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Review
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  8. Article
  9. Spectrum of Clinical and Imaging Features of Children With GFAP Astrocytopathy.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Article
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28 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Roy A QuinlanSchool of Biological and Biomedical Sciences, The University, Durham DH1 3LE, UK. r.a.quinlan@durham.ac.uk
Michael Brenner
James E Goldman
Albee Messing
Columbia University · USDurham University · GBUniversity of Alabama at Birmingham · USUniversity of Wisconsin–Madison · US

Funding

The impact of GFAP mutations upon filament networksP01NS042803 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 2002 to 2012
$11.1M
NINDS NIH HHS NS42803NINDS NIH HHS P01 NS042803
6 · The paper itself

Abstract

Here we review how GFAP mutations cause Alexander disease. The current data suggest that a combination of events cause the disease. These include: (i) the accumulation of GFAP and the formation of characteristic aggregates, called Rosenthal fibers, (ii) the sequestration of the protein chaperones alpha B-crystallin and HSP27 into Rosenthal fibers, and (iii) the activation of both Jnk and the stress response. These then set in motion events that lead to Alexander disease. We discuss parallels with other intermediate filament diseases and assess potential therapies as part of this review as well as emerging trends in disease diagnosis and other aspects concerning GFAP.

Indexed as

Alexander DiseaseAnimalsAstrocytesBrainGenetic Predisposition to DiseaseGlial Fibrillary Acidic ProteinHumansInclusion BodiesIntermediate FilamentsMolecular ChaperonesMutationGlial Fibrillary Acidic ProteinMolecular Chaperones

Identifiers

PMID17498694
PMCPMC2702672
OpenAlexW2120412594

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.