Evidence map›Paper›PMID 41580571›Full record

ArticleActa neuropathologica2026

Pathological insights into cerebral amyloid angiopathy underlying intracerebral haemorrhage: population-based autopsy study.

Ya Su, Mark A Rodrigues, Neshika Samarasekera, James J M Loan, Alice Hosking, Tom J Moullaali, Catherine A Humphreys, Karina McDade, Tracey Millar, Joanna M Wardlaw and 4 more

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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

14 authors.

Ya SuCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Mark A RodriguesCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Neshika SamarasekeraCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
James J M LoanCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Alice HoskingCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Tom J MoullaaliCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Catherine A HumphreysCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Karina McDadeCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Tracey MillarCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Joanna M WardlawCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
Xin ChengDepartment of Neurology, National Centre for Neurological Disorders, National Clinical Research Centre for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Susanne J van VeluwBHF-UKDRI Centre for Vascular Dementia Research, The University of Edinburgh, Edinburgh, UK.
Rustam Al-Shahi SalmanCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK. rustam.al-shahi@ed.ac.uk.
Colin SmithCentre for Clinical Brain Sciences, Institute for Neuroscience and Cardiovascular Research, The University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.

Funding

Medical Research Council G0900428, G1002605Shanghai "Rising Stars of Medical Talents" Youth Development Program SHWSRS(2023)_062Stroke Association SA SCLM 23\100002Stroke Association TSA PPA2017/01Wellcome TrustWellcome Trust 203699/Z/16/ZWellcome Trust 214145/Z/18/Z
6 · The paper itself

Abstract

Lobar intracerebral haemorrhage (ICH) is associated with cerebral amyloid angiopathy (CAA) pathology. Uncertainty remains about the mechanisms leading from CAA to ICH. We investigated the distribution and characteristics of CAA, and its clinical and neuropathological associations. Participants underwent research autopsy in the Lothian IntraCerebral Haemorrhage, Pathology, Imaging and Neurological Outcome (LINCHPIN) study. Neuropathologists rated tissue for CAA using standardised consensus criteria, as well as non-amyloid small vessel disease, Thal phase, and Braak stage. We compared the presence, distribution, and severity of CAA among different brain regions, and in the lobe or hemisphere affected by lobar ICH to corresponding contralateral regions. We evaluated the diagnostic accuracy of Vonsattel CAA grade on a post-mortem cortical specimen (simulating surgical biopsy) versus the reference standard of moderate-to-severe parenchymal CAA at autopsy. Among 162 participants, parenchymal CAA, meningeal CAA, and CAA-associated vasculopathy were diffusely distributed among all cerebral lobes irrespective of the ICH location, but capillary CAA showed an occipital predominance. In lobar ICH, all CAA measures did not differ between the ICH lobe or hemisphere and the contralateral unaffected region. CAA measures did not increase with age, but they were higher in carriers of APOE ε2 or ε4 alleles and in individuals with higher Thal phase or Braak stage. Using a rule-out category of Vonsattel grade ≥ 1 to diagnose CAA on a simulated cortical biopsy achieved 100% sensitivity (95%CI 93.4-100), and a rule-in category of Vonsattel grade ≥ 2 had 79.5% specificity (95%CI 63.5-90.7) versus the reference standard. The distribution and severity of parenchymal CAA, meningeal CAA, and CAA-associated vasculopathy are diffuse regardless of ICH location, indicating the need to better understand the factors underlying bleeding in CAA-affected vessels.

Indexed as

BrainCerebral Amyloid AngiopathyCerebral HemorrhageAgedAged, 80 and overAutopsyFemaleHumansMaleCerebral Amyloid AngiopathyIntracerebral HaemorrhagePathologyPost-mortem Autopsy

Identifiers

PMID41580571
PMCPMC12831695

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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.