Evidence map›Paper›PMID 41945879›Full record

ArticleNeurology2026

Extent of Tau and Its Cognitive Implications in Patients With Cerebral Amyloid Angiopathy Without Cognitive Impairment.

Elif Gokcal, John Alex Becker, Mitchell J Horn, Alvin S Das, Anand Viswanathan, Jonathan Rosand, Jonathan R Polimeni, Reisa Anne Sperling, Keith A Johnson, Steven M Greenberg and 1 more

Abstract read
In one paragraph

Article in 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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0cells of the map it votes in
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

11 authors.

Elif GokcalJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0009-0009-2264-1603
John Alex BeckerDepartment of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-7435-1338
Mitchell J HornJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Alvin S DasDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-2313-977X
Anand ViswanathanJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-5398-1816
Jonathan RosandDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-1014-9138
Jonathan R PolimeniDepartment of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Reisa Anne SperlingDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-1535-6133
Keith A JohnsonDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-5916-6043
Steven M GreenbergJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-1792-8887
M Edip GurolJ. Philip Kistler Hemorrhagic Stroke Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-2169-4457

Funding

Vascular Dysfunction in Cerebral Amyloid AngiopathyR01AG026484 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2005 to 2019
$7.5M
CEREBRAL AMYLOID ANGIOPATHY AND MECHANISMS OF BRAIN AMYLOID ACCUMULATIONR01NS096730 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BACSKAI, BRIAN J, GREENBERG, STEVEN M · 2016 to 2020
$5.7M
Molecular and Physiological Mechanisms of Hypertensive Cerebral MicroangiopathyR01NS114526 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2020 to 2024
$4.4M
Molecular Neuroimaging of Disease Mechanisms in Cerebral Amyloid AngiopathyK23NS083711 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2014 to 2018
$988k
NIA NIH HHS R01 AG026484NINDS NIH HHS K23 NS083711NINDS NIH HHS R01 NS096730NINDS NIH HHS R01 NS114526
6 · The paper itself

Abstract

BACKGROUND AND

objectivesDespite a well-established amyloid-tau neurodegeneration cascade in Alzheimer disease (AD), the extent and mechanistic relevance of tau pathology in cerebral amyloid angiopathy (CAA), a disease of vascular amyloid deposition, remain unclear. Focusing on patients with CAA without cognitive impairment to minimize concurrent AD pathology, we hypothesized that tau extent would be greater in patients with CAA than in healthy controls (HCs), largely attributable to amyloid burden, but it would not be associated with CAA-related imaging markers or cognitive scores in CAA.

methodsThis cross-sectional study included patients with CAA and age-matched and sex-matched HCs, none of whom had cognitive impairment or dementia. All participants underwent brain MRI, Pittsburgh compound B (PiB)-PET for amyloid, and

resultsThe mean age of patients with CAA (n = 50) was 70.3 ± 7.6 years and of HCs was 69.7 ± 7.5 years ( DISCUSSION: Our results suggest that tau extent is mainly driven by age and vascular amyloid among patients with CAA and that tau extent is not related to CAA-related imaging markers or cognitive scores. These findings further support the view that tau does not affect CAA-specific disease mechanisms among patients with CAA without cognitive impairment.

Indexed as

BrainCerebral Amyloid AngiopathyCognitiontau ProteinsAgedAniline CompoundsCognitive DysfunctionCross-Sectional StudiesFemaleHumansMagnetic Resonance ImagingMalePositron-Emission TomographyThiazolesAniline Compoundstau ProteinsThiazoles

Identifiers

PMID41945879
PMCPMC13539575

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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.