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Abstract

Background

Aneurysmal subarachnoid hemorrhage (aSAH) is a relatively uncommon but high mortality form of stroke that can result in long-lasting disability. A better understanding of key neuroinflammatory changes during the early phase (< 72 h) may provide potential avenues of treatment.

Methods

In an attempt to understand these early changes, we recruited 7 aSAH patients for profiling of longitudinal plasma and cerebrospinal fluid (CSF) proteins at up to 72 h post injury. We additionally compared this to control plasma obtained previously from healthy elderly volunteers. Using the Alamar Biosciences NULISAseq platform, we obtained a comprehensive picture of early peripheral and central inflammatory changes after injury.

Results

This study demonstrated very early plasma changes across 107 inflammatory proteins, 22 of which showed significant correlations between plasma and CSF. Of these, CXCL12, IL-15, and SAA1 are detectably elevated < 24 h in plasma, significantly correlated with CSF levels, and altered as a function of aSAH progression over time during this early phase.

Conclusion

This study demonstrates the feasibility of measuring a large number of inflammatory proteins in CSF and plasma from aSAH patients soon after injury. Despite the small sample size and limitations of the control group, we identified several previously reported “hits” that may offer prognostic utility and/or therapeutic potential for aSAH patients: CXCL12, IL-15, and SAA1.

Document Type

Article

Publication Date

2025

Notes/Citation Information

1052-3057/© 2025 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Digital Object Identifier (DOI)

https://doi.org/10.1016/j.jstrokecerebrovasdis.2025.108304

Funding Information

This work was supported by a pilot grant from the National Center for Research Resources (NCRR) and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health (NIH), through Grant UL1TR001998 (LVE, JF, KH); by National Institute on Aging (NIA) training grant T32AG078110 (CSB, LVE) and the UK-ADRC P30 AG072946 (LVE). We thank Dr. Erin Abner for assistance with identifying the control plasma samples, and Ms. Tiffany Lee for performing the Simoa NfL assays. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

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