Evidence map›Paper›PMID 41402627›Full record

ArticleJournal of neurology2025

Plasma p-Tau217 and GFAP predict widespread cognitive decline in Alzheimer's disease.

Núria Guillén, Diana Esteller, Jordi Sarto, Iria Perales, Jose Ríos-Guillermo, Miquel Massons, Isabel Martín-Sobrino, Josep Maria Augé, Laura Naranjo, Raquel Ruiz-García and 16 more

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Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

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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

26 authors.

Núria Guillén *Alzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.ORCID http://orcid.org/0000-0002-1341-9834
Diana Esteller *Alzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Jordi SartoAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Iria PeralesDepartment of Clinical Pharmacology; Medical Statistics Core Facility; Biostatistics Unit, Faculty of Medicine, Hospital Clínic de Barcelona; FRCB-IDIBAPS; Universitat Autònoma de Barcelona, Barcelona, Spain.
Jose Ríos-GuillermoDepartment of Clinical Pharmacology; Medical Statistics Core Facility; Biostatistics Unit, Faculty of Medicine, Hospital Clínic de Barcelona; FRCB-IDIBAPS; Universitat Autònoma de Barcelona, Barcelona, Spain.
Miquel MassonsAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Isabel Martín-SobrinoAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Josep Maria AugéBiochemistry and Molecular Genetics Department, Hospital Clínic de Barcelona, Barcelona, Spain.
Laura NaranjoBiochemistry and Molecular Genetics Department, Hospital Clínic de Barcelona, Barcelona, Spain.
Raquel Ruiz-GarcíaImmunology Service, Biomedical Diagnostic Center, Hospital Clínic de Barcelona, Barcelona, Spain.
Jordi Juncà-ParellaAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Axel RigolAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Victor PatricioAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Adrià Tort-MerinoAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Guadalupe Fernandez-VillullasAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Desirée AlconAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Aina Comas-AlbertíAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Anna AntonellAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Sergi Borrego-ÉcijaAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Marta SánchezAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Magdalena CastellvíAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Beatriz BoschAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Raquel Sánchez-ValleAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Mircea BalasaAlzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Neus Falgàs *Alzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain.
Albert Lladó *Alzheimer's Disease and Other Cognitive Disorders Unit, Hospital Clínic de Barcelona, FRCB-IDIBAPS, Barcelona, Spain. allado@clinic.cat.ORCID http://orcid.org/0000-0002-5066-4150

Funding

Alzheimer's Association AACSF_21_723056Instituto de Salud Carlos III FI20/00076Instituto de Salud Carlos III JR22/00014Instituto de Salud Carlos III PI19/00449Instituto de Salud Carlos III PI23/00173
6 · The paper itself

Abstract

introductionProgression in Alzheimer's disease (AD) involves three main interrelated biological axes-tau deposition, neurodegeneration, and neuroinflammation-that jointly drive cognitive decline. Although several cerebrospinal fluid (CSF) and plasma biomarkers along these axes are well validated for diagnosis, their value for prognosis remains uncertain. We assessed how baseline markers of each axis predict cognitive trajectories in biomarker-confirmed AD.

methodsWe included 136 A + T + N + individuals (median follow-up = 24 months [IQR 12-24]; mean = 17.6 months [SD = 12.4]). Tau-deposition markers (CSF p-Tau181; plasma p-Tau181 and p-Tau217), neurodegeneration markers (CSF t-Tau; CSF and plasma neurofilament light chain, NfL) and a neuroinflammation marker (plasma glial fibrillary acidic protein, GFAP) were quantified using CLEIA, ELISA or Simoa, and stratified into tertiles. Participants were classified by age at onset, clinical phenotype, and APOE ε4 status. Cognition was assessed annually with a comprehensive neuropsychological battery. Linear mixed-effects models (MMRM) were used to test biomarker-cognition associations and interactions with clinical variables.

resultsElevated CSF p-Tau181 and NfL levels were associated with greater decline in memory and executive function. Among plasma biomarkers, p-Tau217 and GFAP showed the strongest associations with widespread cognitive decline, particularly in language, visuospatial, and executive domains. These associations were independent of age at onset, clinical phenotype, and APOE ε4 status. DISCUSSION/

conclusionOur findings highlight the potential prognostic value of fluid biomarkers in AD, especially CSF p-Tau181 and NfL, and plasma p-Tau217 and GFAP. These results suggest promise for improving disease monitoring, although prognostic utility at the individual level remains uncertain.

Indexed as

Alzheimer DiseaseCognitive DysfunctionGlial Fibrillary Acidic Proteintau ProteinsAgedAged, 80 and overBiomarkersDisease ProgressionFemaleHumansLongitudinal StudiesMaleMiddle AgedNeurofilament ProteinsNeuropsychological TestsBiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humanneurofilament protein LNeurofilament Proteinstau ProteinsAlzheimer’s diseaseCognitive declineGFAPPlasma biomarkersPrognosisP-Tau217

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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.