Evidence map›Paper›PMID 39666067›Full record

ArticleJournal of neurology2024

Myelin basic protein and TREM2 quantification in the CSF of patients with Multiple System Atrophy and other Parkinsonian conditions.

Fabian Maass, Sezgi Canaslan, Christoph van Riesen, Peter Hermann, Matthias Schmitz, Claudia Schulte, Kathrin Brockmann, Matthis Synofzik, Mathias Bähr, Inga Zerr

Abstract read
In one paragraph

Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
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  7. Observational
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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

10 authors.

Fabian MaassDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany. fabian.maass@med.uni-goettingen.de.ORCID http://orcid.org/0000-0002-4077-2852
Sezgi CanaslanDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Christoph van RiesenDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Peter HermannDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Matthias SchmitzDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Claudia SchulteHertie Institute for Clinical Brain Research and Center of Neurology, Department of Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Kathrin BrockmannHertie Institute for Clinical Brain Research and Center of Neurology, Department of Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Matthis SynofzikHertie Institute for Clinical Brain Research and Center of Neurology, Department of Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.
Mathias BährDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.
Inga ZerrDepartment of Neurology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is well known that myelin disruption and neuroinflammation are early and distinct pathological hallmarks in multiple system atrophy (MSA) as well as in idiopathic Parkinson's disease and in other atypical Parkinsonian syndromes. The objective of this study was to assess the value of non-neuronal biomarker candidates that reflect myelin disruption and neuroinflammation.

methodsMyelin basic protein (MBP) and the soluble form of TREM2 were quantified in a comprehensive movement disorder cohort from two different neurological centers, comprising a total of 171 CSF samples. Commercially available ELISA systems were employed for quantification.

resultsThe results of the MBP analysis revealed a significant increase in cerebrospinal fluid (CSF) MBP levels in all atypical Parkinsonian conditions compared to PD. This differentiation was more pronounced in the MSA-c subtype compared to MSA-p. Receiver operating characteristic (ROC) analysis revealed a significant discrimination between PD and MSA (p = 0.032, AUC = 0.70), PD and DLB (p = 0.006, AUC = 0.79) and PD and tauopathies (p = 0.006, AUC = 0.74). The results of the TREM2 analysis demonstrated no significant differences between the PD and atypical Parkinsonian groups if not adjusted for confounders. After adjusting for age, sex, and disease duration, the PD group exhibited significantly higher TREM2 levels compared to the DLB group (p = 0.002).

conclusionsIn conclusion, MBP, but not TREM2, is elevated in the CSF of not only MSA but in all atypical Parkinsonian conditions compared to idiopathic Parkinson's disease. This highlights the value of the evaluation of myelin/oligodendrocyte-associated markers in neurodegenerative movement disorders.

Indexed as

BiomarkersMembrane GlycoproteinsMultiple System AtrophyMyelin Basic ProteinReceptors, ImmunologicAgedAged, 80 and overCohort StudiesFemaleHumansMaleMiddle AgedParkinson DiseaseParkinsonian DisordersBiomarkersMBP protein, humanMembrane GlycoproteinsMyelin Basic ProteinReceptors, ImmunologicTREM2 protein, humanBiomarkerCerebrospinal fluidMultiple system atrophyMyelin basic proteinTREM2

Identifiers

PMID39666067
PMCPMC11638341

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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.