Evidence map›Paper›PMID 33661357›Full record

ArticleJournal of neurology2021

The levels of the serine protease HTRA1 in cerebrospinal fluid correlate with progression and disability in multiple sclerosis.

Simone Hjæresen, Tobias Sejbaek, Marcus Axelsson, Helle Vinsløv-Jensen, Sif Kløvedal Mortensen, Gorm Pihl-Jensen, Lenka Novakova, Julie Damgaard Rosgaard Christensen, Christian Bonde Pedersen, Bo Halle and 7 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. 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

17 authors at 3 institutions in 2 countries.

Simone HjæresenDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.ORCID http://orcid.org/0000-0001-6000-4773
Tobias SejbaekDepartment of Regional Health Research, University of Southern Denmark, 5000, Odense, Denmark.ORCID http://orcid.org/0000-0002-7682-2188
Marcus AxelssonDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, and Department of Neurology, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-2036-4007
Helle Vinsløv-JensenDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.
Sif Kløvedal MortensenDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.
Gorm Pihl-JensenDepartment of Neurology, University of Copenhagen, Rigshospitalet Glostrup, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-2596-9358
Lenka NovakovaDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, and Department of Neurology, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Julie Damgaard Rosgaard ChristensenDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.
Christian Bonde PedersenDepartment of Neurosurgery, Clinical Institute, University of Southern Denmark, Odense University Hospital, Odense, Denmark.
Bo HalleDepartment of Neurosurgery, Clinical Institute, University of Southern Denmark, Odense University Hospital, Odense, Denmark.ORCID http://orcid.org/0000-0001-9930-4490
Frantz Rom PoulsenDepartment of Neurosurgery, Clinical Institute, University of Southern Denmark, Odense University Hospital, Odense, Denmark.ORCID http://orcid.org/0000-0001-5715-6901
Jette Lautrup FrederiksenDepartment of Neurology, University of Copenhagen, Rigshospitalet Glostrup, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-1661-7438
Mengliang ZhangDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.ORCID http://orcid.org/0000-0001-5945-6625
Eirikur BenedikzFaculty of Health Sciences, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.ORCID http://orcid.org/0000-0001-6789-8837
Jan LyckeDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, and Department of Neurology, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-7891-8466
Zsolt IllesDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark.ORCID http://orcid.org/0000-0001-9655-0450
Åsa Fex SvenningsenDepartment of Molecular Medicine- Neurobiology Research, University of Southern Denmark, J.B. Winsløws Vej 21, 5000, Odense, Denmark. aasvenningsen@health.sdu.dk.ORCID http://orcid.org/0000-0002-5651-265X
University of Southern Denmark · DKSahlgrenska University Hospital · SEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh Temperature Requirement Serine Protease A1 (HTRA1) degrades extracellular matrix molecules (ECMs) and growth factors. It interacts with several proteins implicated in multiple sclerosis (MS), but has not previously been linked to the disease.

objectiveInvestigate the levels of HTRA1 in cerebrospinal fluid (CSF) in different subtypes of MS and brain tissue.

methodsUsing ELISA, HTRA1 levels were compared in CSF from untreated patients with relapsing-remitting MS (RRMS, n = 23), secondary progressive MS (SPMS, n = 26) and healthy controls (HCs, n = 26). The effect of disease modifying therapies (DMTs) were examined in both patient groups. Cellular distribution in human brain was studied using immunochemistry and the oligointernode database, based on a single-nuclei RNA expression map.

resultsHTRA1 increased in RRMS and SPMS compared to HCs. DMT decreased HTRA1 levels in both types of MS. Using ROC analysis, HTRA1 cut-offs could discriminate HCs from RRMS patients with 100% specificity and 82.6% sensitivity. In the brain, HTRA1 was expressed in glia and neurons.

conclusionHTRA1 is a promising CSF biomarker for MS correlating with disease- and disability progression. Most cell species of the normal and diseased CNS express HTRA1 and the expression pattern could reflect pathological processes involved in MS pathogenesis.

Indexed as

Multiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingBiomarkersCase-Control StudiesDisease ProgressionHigh-Temperature Requirement A Serine Peptidase 1HumansBiomarkersHigh-Temperature Requirement A Serine Peptidase 1HTRA1 protein, humanBiomarkerCerebrospinal fluidDegenerationDimethyl fumarateHTRA1MitoxantroneMultiple sclerosisSecondary progression

Identifiers

PMID33661357
OpenAlexW3133746072

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.