Evidence map›Paper›PMID 29404650›Full record

ReviewDer Nervenarzt2018

[Coagulation factors and multiple sclerosis : Key factors in the pathogenesis?]

K Göbel, C Kleinschnitz, S G Meuth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Nervenarzt, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

3 authors at 2 institutions in 1 country.

K GöbelKlinik für Allgemeine Neurologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland. kerstin.goebel@ukmuenster.de.
C KleinschnitzKlinik für Neurologie, Universitätsklinikum Essen, Hufelandstr. 55, 45147, Essen, Deutschland.
S G MeuthKlinik für Allgemeine Neurologie, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.
Klinik und Poliklinik für Neurologie · DEUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental factors and genetic predisposition influence the individual risk to develop multiple sclerosis (MS). Preclinical results in animal models of MS, such as experimental autoimmune encephalomyelitis (EAE), prove a significant contribution of the corpuscular and plasmatic coagulation system for the severity of MS. It was recently shown that key molecules of the coagulation cascade, such as fibrinogen, thrombin and factor XII can influence neuroinflammatory disorders such as MS. The inhibition of both fibrinogen and factor XII led to a significantly improved disease course in animal models. Furthermore, in patients suffering from MS a dysregulation of diverse coagulation factors was demonstrated. The precise role of these changes for the pathogenesis of MS remains to be clarified. Nonetheless, the identification of molecular mechanisms between inflammation and the coagulation cascade might provide completely new perspectives for the therapy of MS; however, as most of the currently available data were obtained from animal models, this knowledge must be interpreted with an adequate degree of caution.

Indexed as

Blood Coagulation FactorsMultiple SclerosisAnimalsDisease Models, AnimalDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalHumansBlood Coagulation FactorsAutoimmune diseasesCoagulation factorsExperimental autoimmune encephalomyelitisImmunomodulationSide effects

Identifiers

PMID29404650
OpenAlexW2793634804

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.