Evidence map›Paper›PMID 41557565›Full record

ArticleDementia and geriatric cognitive disorders2026

Limited Diagnostic Performance of Cerebrospinal Fluid Glial Fibrillary Acidic Protein in Dementia.

Pontus Erickson, Tobias Borgh Skillbäck, Silke Kern, Ingmar Skoog, Linus Jönsson, Ulf Andreasson, Kaj Blennow, Maria Eriksdotter, Henrik Zetterberg

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In one paragraph

Article in Dementia and geriatric cognitive disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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.

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

9 authors.

Pontus EricksonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden, pontus.eriksson@gu.se.
Tobias Borgh SkillbäckDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Silke KernDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Ingmar SkoogDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Linus JönssonDivision of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Solna, Sweden.
Ulf AndreassonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Maria EriksdotterDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Flemingsberg, Huddinge, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCerebrospinal fluid (CSF) glial fibrillary acidic protein (GFAP) is a neuroinflammatory marker reflecting reactive astrogliosis and is measured regularly in clinical practice. However, its diagnostic utility in differentiating dementia subtypes remains unclear. This study aimed to evaluate differences in CSF GFAP concentrations and its associations with markers of disease severity and amyloid pathology.

methodsWe conducted a retrospective cohort study using three datasets encompassing a broad range of dementia diagnoses. Included variables were CSF GFAP, β-amyloid 42 (Aβ42), the Aβ42/Aβ40 ratio, Mini-Mental State Examination (MMSE) scores, and time from sampling to death.

resultsA total of 1,345 individuals were included. In Parkinson's disease dementia (PDD) and Lewy body dementia, GFAP levels were similar (p > 0.05). Lower levels were observed in PDD compared to early-onset Alzheimer's disease (EAD), late-onset AD (LAD), and vascular dementia (VaD) (all p < 0.05); however, the discriminative performance was low-to-moderate: PDD versus LAD (AUROC = 0.74, CI = 0.64-0.84, p < 0.001), VaD (AUROC = 0.71, CI =0.61-0.81, p < 0.001) and EAD (AUROC = 0.59, CI = 0.47-0.71, p = 0.13). Associations were seen with MMSE in mixed AD and VaD (p = 0.027), but not in the other diagnostic categories. GFAP levels did not differ between subjects grouped according to Aβ42/Aβ40 status (p > 0.05).

conclusionCSF GFAP did not exhibit clinically relevant diagnostic or prognostic value in dementia. Further studies are needed to clarify its role in PDD.

Indexed as

Alzheimer’s diseaseAβ42/40Glial fibrillary acidic proteinParkinson’s diseaseVascular dementia

Identifiers

PMID41557565
PMCPMC12975142

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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.