Evidence map›Paper›PMID 42237156›Full record

ArticleAnnals of neurology2026

Plasma Amyloid Beta and Tau Associations with Cerebral Amyloid Angiopathy Presence and Severity.

Francesco Bax, Lei Liu, Thijs Wijnzen van Harten, Elif Gokcal, Mitchell Jacob Horn, Andrew Warren, Adriana Saba, Zahra Shirzadi, Zora Y DiPucchio, Kristin M Schwab and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

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0citing papers in PubMed
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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

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

14 authors.

Francesco Bax *J.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0003-1725-1175
Lei Liu *Department of Neurology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA.
Thijs Wijnzen van HartenJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0002-3408-9379
Elif GokcalJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0009-0009-2264-1603
Mitchell Jacob HornJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0002-8249-5793
Andrew WarrenJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Adriana SabaDepartment of Neurology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA.
Zahra ShirzadiDepartment of Neurology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0001-6854-9356
Zora Y DiPucchioJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Kristin M SchwabJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Mahmut Edip GurolJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Anand ViswanathanJ.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Jasmeer P Chhatwal *Department of Neurology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0002-7792-1698
Steven Mark Greenberg *J.P. Kistler Hemorrhagic Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID https://orcid.org/0000-0003-1792-8887

Funding

Molecular and Physiological Mechanisms of Hypertensive Cerebral MicroangiopathyR01NS114526 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2020 to 2024
$4.4M
Plasma tau and neurodegenerative markers as predictors of rate of AD progressionR01AG071865 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI CHHATWAL, JASMEER P · 2021 to 2025
$4.2M
NIA NIH HHS R01 AG071865NIH R01AG071865NINDS NIH HHS R01 NS114526
6 · The paper itself

Abstract

objectiveThe aim was to determine whether plasma amyloid beta (Aβ) Aβ37, Aβ40, Aβ42, and p-tau217 differ in cerebral amyloid angiopathy (CAA) from controls and associate with specific magnetic resonance imaging (MRI) markers of CAA.

methodsSingle center hospital-based study (Massachusetts General Hospital) enrolling patients with probable or definite CAA per Boston 2.0 criteria among consecutive individuals presenting with spontaneous intracerebral hemorrhage (ICH) and non-acute ICH related symptoms. Control participants were identified among individuals 55 years or older without history of ICH attending outpatient clinics in the same catchment area and time as the CAA cases. Primary outcome tested whether plasma Aβ37, Aβ40, Aβ42, and p-tau217 differ between patients with CAA and controls. Secondary outcome evaluated the correlation with the severity of selected CAA neuroradiological hallmarks on brain MRI scans obtained within 1 year of sample collection.

resultsA total of 186 patients with CAA (mean age, 71.2 ± 8.3 years; males, 107 [58%]) and 401 controls (mean age, 73.9 ± 8.3 years; males, 211 [53%]) were included in the study. CAA cases had lower Aβ40 (β = -0.60, 95% CI = -0.80 to -0.40, P < 0.001), Aβ42 (β = -0.48, 95% CI = -0.70 to -0.27, P < 0.001), and higher p-tau217 (β = 0.73, 95 %CI = 0.54 to 0.91, P < 0.001) concentrations compared to controls. Aβ40 was the only fragment reduced independent of ptau217 levels. Within the CAA group, biomarkers were associated with both hemorrhagic (reduced Aβ42 with cortical superficial siderosis) and non-hemorrhagic (reduced Aβ40 and Aβ42 with enlarged perivascular spaces in centrum semiovale, reduced Aβ37 and increased p-tau217 with white matter hyperintensities) MRI hallmarks of CAA.

interpretationPlasma Aβ40, Aβ42, and p-tau217 differ between CAA patients and controls and are informative on CAA severity as inferred from brain MRI markers. ANN NEUROL 2026;100:380-390.

Indexed as

Amyloid beta-PeptidesCerebral Amyloid AngiopathyPeptide Fragmentstau ProteinsAgedAged, 80 and overBiomarkersBrainFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedSeverity of Illness IndexAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)BiomarkersPeptide Fragmentstau Proteins

Identifiers

PMID42237156
PMCPMC13387958

What Socratic holds

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Registered trials

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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 Socratic graph.