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Publication Detail
Cerebrospinal fluid metallomics in cerebral amyloid angiopathy: an exploratory analysis.
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Publication Type:Journal article
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Authors:Banerjee G, Forsgard N, Ambler G, Keshavan A, Paterson RW, Foiani MS, Toombs J, Heslegrave A, Thompson EJ, Lunn MP, Fox NC, Zetterberg H, Schott JM, Werring DJ
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Publication date:22/07/2021
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Journal:Journal of Neurology
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Status:Accepted
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Country:Germany
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PII:10.1007/s00415-021-10711-6
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Language:English
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Keywords:Alzheimer’s disease, Cerebral amyloid angiopathy, Cerebrospinal fluid, Ferritin, Iron, Metallomics
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Publisher URL:
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Notes:This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.
Abstract
INTRODUCTION: Cerebral amyloid angiopathy (CAA) is associated with symptomatic intracerebral haemorrhage. Biomarkers of clinically silent bleeding events, such as cerebrospinal fluid (CSF) ferritin and iron, might provide novel measures of disease presence and severity. METHODS: We performed an exploratory study comparing CSF iron, ferritin, and other metal levels in patients with CAA, control subjects (CS) and patients with Alzheimer's disease (AD). Ferritin was measured using a latex fixation test; metal analyses were performed using inductively coupled plasma mass spectrometry. RESULTS: CAA patients (n = 10) had higher levels of CSF iron than the AD (n = 20) and CS (n = 10) groups (medians 23.42, 15.48 and 17.71 μg/L, respectively, p = 0.0015); the difference between CAA and AD groups was significant in unadjusted and age-adjusted analyses. We observed a difference in CSF ferritin (medians 10.10, 7.77 and 8.01 ng/ml, for CAA, AD and CS groups, respectively, p = 0.01); the difference between the CAA and AD groups was significant in unadjusted, but not age-adjusted, analyses. We also observed differences between the CAA and AD groups in CSF nickel and cobalt (unadjusted analyses). CONCLUSIONS: In this exploratory study, we provide preliminary evidence for a distinct CSF metallomic profile in patients with CAA. Replication and validation of these results in larger cohorts is needed.
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