Evidence map›Paper›PMID 40877100›Full record

ArticleThe journal of prevention of Alzheimer's disease2026

Plasma and neurostructural biomarkers in the clinical-biological characterization of early stages of the Alzheimer's disease continuum: findings from the Compostela Aging Study.

Montserrat Zurrón, Arturo Xosé Pereiro, Ana Isabel Rodriguez-Perez, Santiago Galdo-Álvarez, Juan José Ansede, Cristina Lojo-Seoane, Mónica Lindín, David Facal, Miguel Ángel Rivas-Fernández, María Campos-Magdaleno and 3 more

Abstract read
In one paragraph

Article in The journal of prevention of Alzheimer's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 2 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

5 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Amyloid-beta (1-40) peptide is associated with systemic metabolic health.European journal of clinical investigation · 2026
    Article
  5. Article
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

13 authors.

Montserrat ZurrónDepartment of Clinical Psychology and Psychobiology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. Electronic address: montserrat.zurron@usc.es.
Arturo Xosé PereiroDepartment of Developmental Psychology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Ana Isabel Rodriguez-PerezHealth Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain; Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Madrid, Spain.
Santiago Galdo-ÁlvarezDepartment of Clinical Psychology and Psychobiology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Juan José AnsedeFundacion Pública Galega de Medicina Xenomica (SERGAS), National Genotyping Center (CEGEN), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Cristina Lojo-SeoaneDepartment of Developmental Psychology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Mónica LindínDepartment of Clinical Psychology and Psychobiology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
David FacalDepartment of Developmental Psychology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Miguel Ángel Rivas-FernándezDivision of Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles, CA, USA.
María Campos-MagdalenoDepartment of Developmental Psychology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain.
Ángel CarracedoFundacion Pública Galega de Medicina Xenomica (SERGAS), National Genotyping Center (CEGEN), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain; Centre for Biomedical Network Research on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain; Genomic Medicine Group-Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela (USC), Spain.
José Luis Labandeira-GarciaHealth Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain; Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Networking Research Center on Neurodegenerative Diseases (CIBERNED), Madrid, Spain.
Fernando DíazDepartment of Clinical Psychology and Psychobiology, University of Santiago de Compostela (USC), Santiago de Compostela, Spain; Cognitive Neuroscience Research and Psychogerontology Group (NeuCogA-Aging), Institute of Psychology (IPsiUS), USC, Santiago de Compostela, Spain; Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent technical advances in peripheral blood analysis have enabled precise quantification of Alzheimer´s Disease (AD) biomarkers in the early stages of the AD continuum, in an economical, non-invasive and safe manner. The main objective of this study was to contribute to the clinical-biological characterization of the initial stages of cognitive impairment by measurement of blood and neurostructural AD biomarkers in groups of participants classified according to their cognitive clinical phenotype. Plasma concentrations of p-tau217, p-tau181, total tau, neurofilament light chain and amyloid-β 42/40 ratio biomarkers were measured along with APOE gene variants, hippocampal volume and cortical thickness of the AD signature regions. The cohort of 329 participants included Cognitively Unimpaired (CU), Subjective Cognitive Decline (SCD), single-domain amnestic Mild Cognitive Impairment (sd-aMCI), multidomain aMCI (md-aMCI), and single-domain non-amnestic MCI (sd-naMCI) groups. P-tau217 concentrations were significantly higher in the md-aMCI and sd-aMCI groups than in the CU, SCD and sd-naMCI groups. P-tau181 concentrations were significantly higher in md-aMCI group than in CU, SCD and sd-naMCI groups. Hippocampal volume and AD signature cortical thickness were significantly lower in the md-aMCI group than in the CU, SCD and sd-naMCI groups. No across group differences were found in the distribution of carriers/non-carriers of APOE-ε4. Mediation analysis revealed that hippocampal volume and AD signature cortical thickness mediated the relationship between p-tau217 and p-tau181 levels and cognitive performance. Sd-aMCI and md-aMCI represent two distinct and sequential clinical-biological stages of the AD continuum. Conversely, sd-naMCI does not appear to be associated with AD pathology. Finally, the SCD group does not seem to display a higher risk of progression along the AD continuum than the CU group.

Indexed as

AgingAlzheimer DiseaseCognitive Dysfunctiontau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesApolipoproteins EBiomarkersCerebral CortexFemaleHippocampusHumansMagnetic Resonance ImagingMaleNeurofilament ProteinsAmyloid beta-PeptidesApolipoproteins EBiomarkersneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlzheimer´s Disease continuumMild Cognitive ImpairmentNeurostructural biomarkersPlasma biomarkersSubjective Cognitive Decline

Identifiers

PMID40877100
PMCPMC12811771

What OpenQuestion holds

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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.