Evidence map›Paper›PMID 42033997›Full record

ArticleNeurobiology of aging2026

An exploratory analysis of plasma biomarkers associated with cerebral amyloid angiopathy.

Ersin Ersözlü, François Meyer, Lukas Preis, Orkan Arslan, Daria Gref, Louise Droste, Julian Hellmann-Regen, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
PubMed Publisher
In one paragraph

Article in Neurobiology of aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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

5 · Who and what money

Authors and funding

8 authors.

Ersin ErsözlüCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Berlin, Germany. Electronic address: ersin.ersoezlue@charite.de.
François MeyerCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; Neurocognitive Disorders Research Group, GIGA Clinical Neurosciences, University of Liège, Liège, Belgium.
Lukas PreisCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Berlin, Germany.
Orkan ArslanCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany.
Daria GrefCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Berlin, Germany.
Louise DrosteCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Berlin, Germany.
Julian Hellmann-RegenCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Department of Psychiatry and Neurosciences, Hindenburgdamm 30, Berlin 12203, Germany; Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, ECRC Experimental and Clinical Research Center, Lindenberger Weg 80, Berlin 13125, Germany; German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Berlin, Germany.
Alzheimer’s Disease Neuroimaging Initiative

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) remains diagnostically challenging, particularly in asymptomatic individuals. While CAA often co-exists with Alzheimer's disease (AD), it may even have a direct impact on AD pathophysiology and the cognitive decline within the clinical course of AD. While fluid biomarkers are well established for AD pathology, reliable markers to characterize CAA are lacking. We analyzed two subsets of participants from the Alzheimer's Disease Neuroimaging Initiative with available plasma biomarker measurements from a 145-analyte multiplex immunoassay panel: one with T2*-weighted gradient-echo magnetic resonance imaging (MRI) data (n = 21) and another with postmortem neuropathological data (n = 24). We defined CAA as ≥ 2 lobar microbleeds on MRI or moderate-to-severe neocortical amyloid angiopathy on neuropathological examination. Plasma analytes were assessed twice per participant, one year apart, with the earlier sample obtained up to 6.6 years prior to either the first MRI or neuropathological examinations. In both cohorts, various markers related to inflammation, lipid metabolism, and cell adhesion were associated with CAA proxy measures. Specifically, both increased (Fas ligand receptor, Receptor for Advanced Glycosylation End-Products, Osteopontin, and Vascular Cell Adhesion Molecule-1) and decreased (Vitronectin, Endothelial Growth Factor) biomarker levels were associated with lobar microbleeds, while increased apolipoproteins (ApoAII, ApoCI, ApoCIII, ApoE, and clusterin) and decreased AXL were associated with CAA severity in neuropathology. Ratios between inversely associated markers enhanced correlation strength and differed between CAA and non-CAA. Given the small sample sizes in our exploratory analyses, larger studies are required to evaluate the discriminatory potential and clinical translatability of the identified biomarkers for CAA.

Indexed as

Cerebral Amyloid AngiopathyAgedAged, 80 and overAlzheimer DiseaseBiomarkersCohort StudiesFemaleHumansMagnetic Resonance ImagingMaleBiomarkersAlzheimer’s diseaseCerebral amyloid angiopathyCerebral microbleedsNeuropathologyPlasma biomarkers

Identifiers

PMID42033997

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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.