Evidence map›Paper›PMID 42479178›Full record

ArticleActa neuropathologica2026

Cerebral amyloid angiopathy, brain iron concentrations, and cognitive decline in older people.

Sonal Agrawal, Maude Wagner, Sue E Leurgans, Puja Agarwal, Louise van der Weerd, David A Bennett, Ashley I Bush, Scott Ayton, Julie A Schneider

Abstract read
In one paragraph

Article in Acta neuropathologica, 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

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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

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

9 authors.

Sonal AgrawalRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA. sonal_agrawal@rush.edu.ORCID https://orcid.org/0000-0003-2375-8888
Maude WagnerRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA.
Sue E LeurgansRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA.
Puja AgarwalRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA.
Louise van der WeerdDepartment of Radiology & Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA.
Ashley I BushThe Florey Institute of Neuroscience and Mental Health, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3010, Australia.
Scott AytonThe Florey Institute of Neuroscience and Mental Health, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3010, Australia.
Julie A SchneiderRush Alzheimer's Disease Center, Rush University Medical Center, Jelke Building, 1750 W. Harrison Street, Chicago, IL, 60612, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is a common brain pathology in older people and has been recently recognized as a major risk factor for amyloid-related imaging abnormalities during anti-amyloid antibody therapy. CAA pathophysiology may involve iron released from ruptured vessels, but the association between postmortem CAA and brain iron is unclear. This study investigates the association between CAA and brain iron and whether elevated iron modifies the association between CAA and cognitive decline. We studied 626 Rush Memory and Aging Project decedents (mean age at death = 90 [SD = 6.1] years, 70% women) who completed baseline and longitudinal cognitive assessments and underwent detailed neuropathologic evaluation for CAA, Alzheimer's disease neuropathologic changes (ADNC), and other brain pathologies. Brain iron content was assessed from the inferior temporal cortex using Inductively Coupled Plasma Mass Spectrometry (ICP-MS). Linear regression and mixed-effects models were used for analysis. CAA was common: 266 (42%) had mild, 153 (24%) had moderate, and 75 (12%) had severe CAA. In analyses adjusted for demographics, intermediate/high ADNC, and other pathologies, the presence and severity of CAA were associated with elevated cortical brain iron (Est = 0.033, SE = 0.011, p = 0.002; Est = 0.017, SE = 0.004, p < 0.001, respectively). When examining associations with nonlinear cognitive change before death (mean follow-up = 7.7 [SD = 3.9] years), both CAA and elevated iron were independently associated with faster annual rates of decline in global cognition and semantic memory (all p < 0.04). Elevated iron was also associated with faster declines in episodic and working memory and perceptual speed (all p < 0.02). When exploring whether brain iron modulates the association of CAA with cognitive decline, we found that CAA had steeper decline in perceptual speed when elevated iron was present compared to when low iron was present (p = 0.03). Together, these findings suggest that brain iron may contribute to the clinical impact of CAA in older age.

Indexed as

BrainCerebral Amyloid AngiopathyCognitive DysfunctionIronAgedAged, 80 and overAgingFemaleHumansLongitudinal StudiesMaleIronAlzheimer’s diseaseBrain ironCerebral amyloid angiopathyCognitive declineLongitudinal cohort studyMetalSmall vessel disease

Identifiers

PMID42479178
PMCPMC13388426

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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.