Evidence map›Paper›PMID 31838996›Full record

ReviewJournal of neurodevelopmental disorders2019

Refining the concept of GFAP toxicity in Alexander disease.

Albee Messing

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neurodevelopmental disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Leukodystrophy Imaging: Insights for Diagnostic Dilemmas.Medical sciences (Basel, Switzerland) · 2024
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. GFAP at 50.ASN neuro
    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

1 author at 1 institution in 1 country.

Albee MessingWaisman Center and Department of Comparative Biosciences, University of Wisconsin-Madison, 1500 Highland Ave, Rm. 713B, Madison, WI, 53705, USA. amessing@wisc.edu.ORCID 0000-0001-6049-0521
University of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlexander disease is caused by dominantly acting mutations in glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes in the central nervous system. MAIN BODY: In addition to the sequence variants that represent the origin of disease, GFAP accumulation also takes place, together leading to a gain-of-function that has sometimes been referred to as "GFAP toxicity." Whether the nature of GFAP toxicity in patients, who have mixtures of both mutant and normal protein, is the same as that produced by simple GFAP excess, is not yet clear.

conclusionThe implications of these questions for the design of effective treatments are discussed.

Indexed as

Alexander DiseaseAnimalsAstrocytesGlial Fibrillary Acidic ProteinHumansMutationGFAP protein, humanGlial Fibrillary Acidic ProteinAntisense oligonucleotidesAstrocyteGFAP

Identifiers

PMID31838996
PMCPMC6913036
OpenAlexW2995442567

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.