Evidence map›Paper›PMID 40407316›Full record

ArticleEuropean journal of neurology2025

Glial Fibrillary Acid Protein Reflects Disease Activity in Autoimmune Encephalitis.

Johannes Piepgras, Marlene L Piepgras, Falk Steffen, Laura Ehrhardt, Martin A Schaller-Paule, Yavor Yalachkov, Frauke Zipp, Stefan Bittner

Abstract read
In one paragraph

Article in European journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Observational
  2. Review
  3. Article
  4. Review
  5. Neuroglial markers of damage in autoimmune neurology.Therapeutic advances in neurological disorders · 2026
    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

8 authors.

Johannes PiepgrasDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Marlene L PiepgrasMainz, Germany.ORCID 0000-0003-1767-4936
Falk SteffenDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Laura EhrhardtDepartment of Pediatrics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Martin A Schaller-PauleDepartment of Neurology, Goethe University, University Hospital Frankfurt, Frankfurt am Main, Germany.
Yavor YalachkovDepartment of Neurology, Goethe University, University Hospital Frankfurt, Frankfurt am Main, Germany.
Frauke ZippDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Stefan BittnerDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID 0000-0003-2179-3655

Funding

Deutsche Forschungsgemeinschaft 213904703Deutsche Forschungsgemeinschaft 490846870Else Kröner-Fresenius-Stiftung 2019_A72Else Kröner-Fresenius-Stiftung TransMed Jumpstart ProgramHermann und Lilly Schilling-Stiftung für Medizinische Forschung
6 · The paper itself

Abstract

background and purposeManagement of autoimmune encephalitis (AE) is challenging due to a lack of reliable biomarkers. We here assess the combination of glial fibrillary acid protein (GFAP) and neurofilament (NfL) as biomarkers for diagnosis and disease monitoring of AE.

methodsGFAP and NfL CSF levels (cGFAP, cNfL) of 42 AE patients were correlated with CSF markers of neuroinflammation. NfL/GFAP ratios were compared between patients with stable and active AE, stable and active multiple sclerosis (MS), and patients undergoing diagnostic lumbar puncture without evident pathological alterations (controls).

resultsIn patients with AE, cGFAP levels showed strong correlations with albumin and IgG quotients and moderate correlations with CSF cell count; cNfL levels showed weak correlations with albumin quotients. cGFAP and cNfL levels showed no significant differences between patients with and without epileptic activity or inflammatory MRI lesions. Both sNfL and sGFAP correlated with the Clinical Assessment Scale in Autoimmune Encephalitis. Compared to NfL or GFAP alone, the NfL/GFAP ratio from CSF or serum led to a clearer separation of AE from MS patients and controls. Furthermore, serum NfL/GFAP ratios better discriminated active from stable AE.

conclusioncGFAP levels indicate intrathecal inflammatory processes in patients with active AE to a stronger degree than cNfL levels. Serum NfL/GFAP ratios recognize active AE, suggesting this ratio identifies AE patients with CNS-compartmentalized neuronal injury (autoantibody-mediated or cytotoxic) behind a relatively intact blood-brain barrier. Our findings indicate that the NfL/GFAP ratio can function as a blood-based biomarker, aiding clinicians with diagnosis and disease management of AE.

Indexed as

EncephalitisGlial Fibrillary Acidic ProteinHashimoto DiseaseNeurofilament ProteinsAdultAgedBiomarkersFemaleHumansMaleMiddle AgedMultiple SclerosisYoung AdultBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament Proteinsautoimmune encephalitisbiomarkerglial fibrillary acid proteinneurofilamentneuroinflammation

Identifiers

PMID40407316
PMCPMC12100762

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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.