Evidence map›Paper›PMID 39254698›Full record

ArticleJournal of neurology2024

GFAP and NfL as fluid biomarkers for clinical disease severity and disease progression in multiple system atrophy (MSA).

Sabrina Katzdobler, Georg Nübling, Martin Klietz, Urban M Fietzek, Carla Palleis, Alexander M Bernhardt, Florian Wegner, Meret Huber, Sophia Rogozinski, Luisa-Sophie Schneider and 21 more

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 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
–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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Glymphatic dysfunction in cerebellar neurodegeneration: mechanistic insights and emerging clinical implications.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  5. Multiple system atrophy: cure and care.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
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  19. Clinical use and reporting of neurofilament quantification in neurological disorders: A global overview.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  20. 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

31 authors.

Sabrina KatzdoblerDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany.
Georg NüblingDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany.
Martin KlietzDepartment of Neurology, Hanover Medical School, Hanover, Germany.
Urban M FietzekDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany.
Carla PalleisDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany.
Alexander M BernhardtDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany.
Florian WegnerDepartment of Neurology, Hanover Medical School, Hanover, Germany.
Meret HuberDepartment of Neurology, Hanover Medical School, Hanover, Germany.
Sophia RogozinskiDepartment of Neurology, Hanover Medical School, Hanover, Germany.
Luisa-Sophie SchneiderDepartment of psychiatry and neuroscience, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Eike Jakob SpruthGerman Center for Neurodegenerative Diseases (DZNE), Berlin, Germany.
Aline BeyleDepartment of Neurology, University of Bonn, Bonn, Germany.
Ina R VogtGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Bonn, Germany.
Moritz BrandtGerman Center for Neurodegenerative Diseases (DZNE), Dresden, Germany.
Niels HansenDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, University of Goettingen, Goettingen, Germany.
Wenzel GlanzGerman Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany.
Kathrin BrockmannGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Annika SpottkeDepartment of Neurology, University of Bonn, Bonn, Germany.
Daniel C HoffmannGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Bonn, Germany.
Oliver PetersDepartment of psychiatry and neuroscience, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Josef PrillerDepartment of Psychiatry and Psychotherapy, School of Medicine and Health, Technical University of Munich, Munich, Germany.
Jens WiltfangDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, University of Goettingen, Goettingen, Germany.
Emrah DüzelGerman Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany.
Anja SchneiderGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Bonn, Germany.
Björn FalkenburgerGerman Center for Neurodegenerative Diseases (DZNE), Dresden, Germany.
Thomas KlockgetherDepartment of Neurology, University of Bonn, Bonn, Germany.
Thomas GasserGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Brigitte NuscherChair of Metabolic Biochemistry, Faculty of Medicine, Biomedical Center (BMC), LMU Munich, Munich, Germany.
Christian HaassMunich Cluster for Systems Neurology, SyNergy, Munich, Germany.
Günter HöglingerDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany. Guenter.Hoeglinger@med.uni-muenchen.de.
Johannes LevinDepartment of Neurology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany. Johannes.levin@med.uni-muenchen.de.ORCID http://orcid.org/0000-0001-5092-4306

Funding

Deutsche Forschungsgemeinschaft EXC 2145 SyNergy - ID 390857198
6 · The paper itself

Abstract

backgroundMultiple system atrophy (MSA), an atypical parkinsonian syndrome, is a rapidly progressive neurodegenerative disease with currently no established fluid biomarkers available. MSA is characterized by an oligodendroglial α-synucleinopathy, progressive neuronal cell loss and concomitant astrocytosis. Here, we investigate glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) as fluid biomarkers for differential diagnosis, assessment of clinical disease severity and prediction of disease progression in MSA.

methodsGFAP and NfL levels were analyzed in plasma and CSF samples of 47 MSA patients as well as 24 Parkinson's disease (PD) and 25 healthy controls (HC) as reference cohorts. In MSA, biomarker levels were correlated to baseline and longitudinal clinical disease severity (UMSARS scores).

resultsIn MSA, GFAP levels in CSF and plasma predicted baseline clinical disease severity as indicated by UMSARS scores, while NfL levels predicted clinical disease progression as indicated by longitudinal changes in UMSARS scores. Cross-sectionally, NfL levels in CSF and plasma were significantly elevated in MSA compared to both PD and HC. Receiver operating curves (ROC) indicated high diagnostic accuracy of NfL for distinguishing MSA from PD (CSF: AUC = 0.97, 95% CI 0.90-1.00; plasma: AUC = 0.90, 95% CI 0.81-1.00). DISCUSSION: In MSA, GFAP shows promise as novel biomarker for assessing current clinical disease severity, while NfL might serve as biomarker for prediction of disease progression and differential diagnosis of MSA against PD.

Indexed as

BiomarkersDisease ProgressionGlial Fibrillary Acidic ProteinMultiple System AtrophyNeurofilament ProteinsSeverity of Illness IndexAgedCross-Sectional StudiesDiagnosis, DifferentialFemaleHumansMaleMiddle AgedParkinson DiseaseROC CurveBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament ProteinsFluid biomarkersGlial fibrillary acidic proteinMultiple system atrophyNeurofilament light chainNeuroinflammation

Identifiers

PMID39254698
PMCPMC11447157

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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.