Temporal alterations in cerebrospinal fluid amyloid beta-protein and apolipoprotein E after subarachnoid hemorrhage


Kay, Andrew, Petzold, Axel, Kerr, Mary, Keir, Geoff, Thompson, Ed and Nicoll, James (2003) Temporal alterations in cerebrospinal fluid amyloid beta-protein and apolipoprotein E after subarachnoid hemorrhage. Stroke, 34, (12), e240-e243. (doi:10.1161/01.STR.0000100157.88508.2F).

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Description/Abstract

Background and Purpose— The mechanism underlying the association between possession of the APOE{epsilon}4 allele and less favorable outcome after subarachnoid hemorrhage (SAH) remains to be determined. After SAH the level of apolipoprotein E (apoE) in the cerebrospinal fluid (CSF) is decreased, and lower levels are associated with more severe injury and less favorable outcome. This study examined serial CSF samples to determine the time course for the decrease in CSF apoE and the relationship between CSF apoE and amyloid ß-protein (Aß), testing the hypothesis that apoE-Aß interactions occur in vivo after SAH.

Methods— Enzyme-linked immunosorbent assay was used to assay apoE, Aß1–40, and Aß1–42 in serial ventricular CSF samples from 19 patients with SAH and 13 controls. CSF S100B and {tau} were assayed as surrogate markers of brain injury.

Results— There was a sustained decrease in CSF apoE (P<0.001) and Aß (P<0.001) after SAH in contrast to the observed elevation in CSF S100B (P<0.001) and {tau} (P<0.001) concentration. There was significant correlation between CSF Aß concentration and clinical outcome (r=0.65, P<0.01), and the decrease in CSF Aß concentration correlated significantly with that of apoE (r=0.85, P<0.0001).

Conclusions— After SAH both apoE and Aß levels decrease in the CSF, supporting the concept that interactions between these proteins occur in vivo. The possibility that apoE and Aß influence outcome after SAH warrants further investigation.

Item Type: Article
Additional Information: Research report
ISSNs: 0039-2499 (print)
Related URLs:
Keywords: amyloid, apolipoprotein, cerebrospinal fluid, subarachnoid hemorrhage
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Divisions: University Structure - Pre August 2011 > School of Medicine > Clinical Neurosciences
ePrint ID: 27610
Date Deposited: 26 Apr 2006
Last Modified: 27 Mar 2014 18:16
Contact Email Address: J.Nicoll@soton.ac.uk
URI: http://eprints.soton.ac.uk/id/eprint/27610

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