Evidence map›Paper›PMID 38940331›Full record

ArticleBrain : a journal of neurology2024

Association of glial fibrillary acid protein, Alzheimer's disease pathology and cognitive decline.

Débora E Peretti, Cecilia Boccalini, Federica Ribaldi, Max Scheffler, Moira Marizzoni, Nicholas J Ashton, Henrik Zetterberg, Kaj Blennow, Giovanni B Frisoni, Valentina Garibotto

Abstract read
In one paragraph

Article in Brain : a journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  4. Investigating AD and non-AD [European journal of nuclear medicine and molecular imaging · 2026
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  15. The effects of polysaccharides fromHistology and histopathology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Débora E PerettiLaboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocentre and Faculty of Medicine, University of Geneva, Geneva 1205, Switzerland.ORCID 0000-0002-3033-8817
Cecilia BoccaliniLaboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocentre and Faculty of Medicine, University of Geneva, Geneva 1205, Switzerland.
Federica RibaldiLaboratory of Neuroimaging of Aging (LANVIE), University of Geneva, Geneva 1205, Switzerland.ORCID 0000-0001-9208-4472
Max SchefflerDivision of Radiology, Geneva University Hospitals, Geneva 1205, Switzerland.
Moira MarizzoniBiological Psychiatry Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia 25125, Italy.
Nicholas J AshtonCentre for Age-Related Medicine, Stavanger University Hospital, Stavanger 4011, Norway.
Henrik ZetterbergMental Health & Biomedical Research Unit for Dementia, Maudsley NIHR Biomedical Research Centre, London SE5 8AF, UK.ORCID 0000-0003-3930-4354
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal 413 90, Sweden.
Giovanni B FrisoniLaboratory of Neuroimaging of Aging (LANVIE), University of Geneva, Geneva 1205, Switzerland.
Valentina GaribottoLaboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocentre and Faculty of Medicine, University of Geneva, Geneva 1205, Switzerland.ORCID 0000-0003-2422-698X

Funding

Association Suisse pour la Recherche sur la Maladie d'Alzheimer, GenèveFondation AETAS, GenèveFondation Child Care, GenèveFondation Edmond J. Safra, GenèveFondation Minkoff, GenèveFondation Segré, GenèveFondazione Agusta, LuganoMcCall Macbain Foundation, CanadaNicole et René Keller, GenèvePrivate Foundation of Geneva University HospitalsRace Against Dementia Foundation, London, UK
6 · The paper itself

Abstract

Increasing evidence shows that neuroinflammation is a possible modulator of tau spread effects on cognitive impairment in Alzheimer's disease. In this context, plasma levels of the glial fibrillary acidic protein (GFAP) have been suggested to have a robust association with Alzheimer's disease pathophysiology. This study aims to assess the correlation between plasma GFAP and Alzheimer's disease pathology, and their synergistic effect on cognitive performance and decline. A cohort of 122 memory clinic subjects with amyloid and tau PET, MRI scans, plasma GFAP and Mini-Mental State Examination (MMSE) was included in the study. A subsample of 94 subjects had a follow-up MMSE score at ≥1 year after baseline. Regional and voxel-based correlations between Alzheimer's disease biomarkers and plasma GFAP were assessed. Mediation analyses were performed to evaluate the effects of plasma GFAP on the association between amyloid and tau PET and between tau PET and cognitive impairment and decline. GFAP was associated with increased tau PET ligand uptake in the lateral temporal and inferior temporal lobes in a strong left-sided pattern independently of age, sex, education, amyloid and APOE status (β = 0.001, P < 0.01). The annual rate of MMSE change was significantly and independently correlated with both GFAP (β = 0.006, P < 0.01) and global tau standardized uptake value ratio (β = 4.33, P < 0.01), but not with amyloid burden. Partial mediation effects of GFAP were found on the association between amyloid and tau pathology (13.7%) and between tau pathology and cognitive decline (17.4%), but not on global cognition at baseline. Neuroinflammation measured by circulating GFAP is independently associated with tau Alzheimer's disease pathology and with cognitive decline, suggesting neuroinflammation as a potential target for future disease-modifying trials targeting tau pathology.

Indexed as

Alzheimer DiseaseCognitive DysfunctionGlial Fibrillary Acidic ProteinPositron-Emission Tomographytau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersCohort StudiesFemaleHumansMagnetic Resonance ImagingMaleMental Status and Dementia TestsMiddle AgedAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteintau ProteinsAlzheimer’s disease biomarkerscognitive declineglial fibrillary acidic proteinneurofibrillary tau tanglespositron emission tomography

Identifiers

PMID38940331
PMCPMC11629700

What Socratic 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 Socratic graph.