Cited by 186Barrier Structure and Function StudiesIntracerebral and Subarachnoid Hemorrhage ResearchAlzheimer's disease research and treatments

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Neuroinflammation and Blood-Brain Barrier Changes in Capillary Amyloid Angiopathy

Carrano, Anna, Hoozemans, Jeroen J.M., van der Vies, Saskia M., van Horssen, Jack, de Vries, Helga E., Rozemuller, Annemieke J.M.·2012·Neurodegenerative Diseases

DOI 10.1159/000334916

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Abstract

INTRODUCTION: β-Amyloid (Aβ) accumulation in cortical capillaries is a variant of cerebral amyloid angiopathy (CAA) referred to as capillary CAA (capCAA). capCAA is associated with a neuroinflammatory response. In vitro studies indicate that Aβ induces reactive oxygen species (ROS) production, mainly generated through NADPH oxidase (NOX), by activated microglia. ROS in turn can induce altered expression of tight junctions (TJ), which are essential for blood-brain barrier (BBB) function. Whether the function of the BBB is affected in the brains of Alzheimer's disease (AD) patients with comorbid capCAA remains elusive. Cases with capCAA and no other AD-related changes allow studying capCAA-associated BBB alterations independent of AD pathology. AIM: In this study, we have investigated BBB alterations in capCAA and addressed the role of the neuroinflammatory response. METHODS: Human postmortem brain tissue with capCAA was analyzed by immunohistochemical staining. RESULTS: In this study, we show for the first time a dramatic loss of TJ proteins claudin-5, occludin and ZO-1 in Aβ-laden capillaries. In addition, affected capillaries are associated with clusters of NOX-2-positive activated microglia. Disrupted BBB function was observed by increased presence of fibrinogen around the affected capillaries. CONCLUSIONS: Our data provide support for the early observation that neuroinflammatory response is involved in the altered expression of TJs in endothelial cells and loss of BBB integrity in capCAA.

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Authors: Carrano, A., Hoozemans, J. J. M., van der Vies, S. M., van Horssen, J., de Vries, H. E., & Rozemuller, A. J. M.
Affiliations: Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
ORCID: Carrano, Anna
Hoozemans, Jeroen J.M.
Venue: Neurodegenerative Diseases
Publisher: S. Karger AG
Published: 2012
Volume: 10
Issue: 1-4
Pages: 329-331
ISSN: 1660-2854 (ISSN-L)
1660-2862
DOI: 10.1159/000334916
OpenAlex: W1974295585
Cited by: 186
References: 16
Citations by year: 2026: 12 · 2025: 15 · 2024: 19 · 2023: 22 · 2022: 17 · 2021: 29 · 2020: 18 · 2019: 8 · 2018: 11 · 2017: 5 · 2016: 9 · 2015: 2 · 2014: 7 · 2013: 9 · 2012: 1
FWCI: 3.06
Type: journal article
Language: en
Open access: closed
Licence: www.karger.com/Services/SiteLicenses (vor)
www.karger.com/Services/SiteLicenses (tdm)
Locations: Neurodegenerative Diseases (publishedVersion)
PubMed (publishedVersion)
Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
Pure Amsterdam UMC (submittedVersion)
VU Research Portal (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Health Sciences › Medicine › Clinical Neurology › Intracerebral and Subarachnoid Hemorrhage Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Keywords: amyloid-beta, blood-brain barrier, neuroinflammation, tight junctions, claudin-5, occludin, ZO-1, NADPH oxidase, NOX2, microglial activation, reactive oxygen species, fibrinogen, Alzheimer's disease, postmortem brain
MeSH terms: Blood Proteins, Blood-Brain Barrier, Brain, Capillaries, Encephalitis, Fibrinogen, Humans, Membrane Proteins, Phosphoproteins, Cohort Studies, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Tight Junctions, NADPH Oxidases, Claudins, Claudin-5, Occludin, Zonula Occludens-1 Protein

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Neuroinflammation and Blood-Brain Barrier Changes in Capillary Amyloid Angiopathy

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