Evidence map›Paper›PMID 37789345›Full record

ArticleMolecular neurodegeneration2023

Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress.

Ken Uekawa, Yorito Hattori, Sung Ji Ahn, James Seo, Nicole Casey, Antoine Anfray, Ping Zhou, Wenjie Luo, Josef Anrather, Laibaik Park and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
13.0field-weighted citation impact, top 1% of its field
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

58 citing papers in PubMed, 63 citations in OpenAlex.

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  14. Engulfment by brain macrophages in a short-lived vertebrate.bioRxiv : the preprint server for biology · 2026
    Article
  15. Endothelial NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  16. Review
  17. Article
  18. Vascular contribution to cognitive impairment and dementia (VCID): proceedings of 2025 workshop of the Jackson Laboratory.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  19. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Ken UekawaFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Yorito HattoriFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Sung Ji AhnFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
James SeoFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Nicole CaseyFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Antoine AnfrayFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Ping ZhouFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Wenjie LuoFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Josef AnratherFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA.
Laibaik ParkFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA. lap2003@med.cornell.edu.
Costantino IadecolaFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, 10021, USA. coi2001@med.cornell.edu.ORCID http://orcid.org/0000-0001-9797-073X
Cornell University · US

Funding

Overexpression of the amyloid precursor protein and cerebrovascular regulationR01NS037853 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Costantino Iadecola · 1998 to 2026
$10.6M
tPA and Cerebrovascular Regulation in a Model of β-amyloid PathologyR01NS097805 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Laibaik Park · 2018 to 2026
$3.8M
NIH HHS NS37853NINDS NIH HHS R01 NS037853NINDS NIH HHS R01 NS097805
6 · The paper itself

Abstract

backgroundCerebral amyloid angiopathy (CAA) is a devastating condition common in patients with Alzheimer's disease but also observed in the general population. Vascular oxidative stress and neurovascular dysfunction have been implicated in CAA but the cellular source of reactive oxygen species (ROS) and related signaling mechanisms remain unclear. We tested the hypothesis that brain border-associated macrophages (BAM), yolk sac-derived myeloid cells closely apposed to parenchymal and leptomeningeal blood vessels, are the source of radicals through the Aβ-binding innate immunity receptor CD36, leading to neurovascular dysfunction, CAA, and cognitive impairment.

methodsTg2576 mice and WT littermates were transplanted with CD36

resultsThe increase in blood flow evoked by whisker stimulation (functional hyperemia) or by endothelial and smooth muscle vasoactivity was markedly attenuated in WT → Tg2576 chimeras but was fully restored in CD36

conclusionsCD36 deletion in BAM suppresses ROS production and rescues the neurovascular dysfunction and damage induced by Aβ. CD36 deletion in BAM also reduced brain Aβ

Indexed as

Alzheimer DiseaseCerebral Amyloid AngiopathyCognitive DysfunctionAmyloid beta-PeptidesAnimalsBrainHumansMacrophagesMiceMice, TransgenicOxidative StressReactive Oxygen SpeciesAmyloid beta-PeptidesReactive Oxygen SpeciesARIAAβ clearanceBorder-associated macrophagesCD36Neurovascular unit dysfunctionVascular oxidative stress

Identifiers

PMID37789345
PMCPMC10548599
OpenAlexW4387311036

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.