Evidence map›Paper›PMID 33773595›Full record

ArticleAlzheimer's research & therapy2021

Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment.

Claudia Cicognola, Shorena Janelidze, Joakim Hertze, Henrik Zetterberg, Kaj Blennow, Niklas Mattsson-Carlgren, Oskar Hansson

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 6 pooled it
26.8field-weighted citation impact, top 1% 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

181 citing papers in PubMed, 6 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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  9. Japan-Multimodal Intervention Trial for the Prevention of Dementia: A randomized controlled trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  12. APOE ε4 accelerates plasma p-tau217 trajectory: a Bayesian joint longitudinal analysis of ADNI.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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121 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 2 countries.

Claudia CicognolaClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden. claudia.cicognola@med.lu.se.ORCID 0000-0003-1806-7089
Shorena JanelidzeClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Joakim HertzeMemory Clinic, Skåne University Hospital, Malmö, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Niklas Mattsson-CarlgrenClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden. oskar.hansson@med.lu.se.
Lund University · SESahlgrenska University Hospital · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPlasma glial fibrillary acidic protein (GFAP) is a marker of astroglial activation and astrocytosis. We assessed the ability of plasma GFAP to detect Alzheimer's disease (AD) pathology in the form of AD-related amyloid-β (Aβ) pathology and conversion to AD dementia in a mild cognitive impairment (MCI) cohort.

methodOne hundred sixty MCI patients were followed for 4.7 years (average). AD pathology was defined using cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology.

resultsBaseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. When also including APOE ε4 status as a predictor, the accuracy of the model to detect abnormal CSF Aβ42/40 status improved (AUC = 0.86, p = 0.02). Plasma GFAP predicted subsequent conversion to AD dementia with an AUC of 0.84 (95% CI 0.77-0.91), which was not significantly improved when adding APOE ε4 or age as predictors to the model. Longitudinal GFAP slopes for Aβ-positive and MCI who progressed to dementia (AD or other) were significantly steeper than those for Aβ-negative (p = 0.007) and stable MCI (p < 0.0001), respectively.

conclusionPlasma GFAP can detect AD pathology in patients with MCI and predict conversion to AD dementia.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesBiomarkersGlial Fibrillary Acidic ProteinHumansPeptide Fragmentstau ProteinsAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinPeptide Fragmentstau ProteinsAlzheimer’s diseaseBlood biomarkersGFAPMild cognitive impairment

Identifiers

PMID33773595
PMCPMC8005231
OpenAlexW3152459827

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.