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Stroke. 2003;34:e240-e243
Published online before print November 6, 2003, doi: 10.1161/01.STR.0000100157.88508.2F
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(Stroke. 2003;34:e240.)
© 2003 American Heart Association, Inc.


Research Reports

Temporal Alterations in Cerebrospinal Fluid Amyloid ß-Protein and Apolipoprotein E After Subarachnoid Hemorrhage

Andrew Kay, MBBS; Axel Petzold, PhD; Mary Kerr, PhD; Geoff Keir, PhD; Ed Thompson, DSc James Nicoll, MD

From the Department of Neurosurgery, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK (A.K.); Department of Neuroimmunology, University of London, Institute of Neurology and Neurosurgery, London, UK (A.P., G.K., E.T.); Department of Neurosurgery and Center for Nursing Research, University of Pittsburgh, Pittsburgh, Pa (M.K.); and Division of Clinical Neurosciences, University of Southampton, Southampton General Hospital, Southampton, UK (J.N.).

Correspondence to Andrew Kay, MBBS, Department of Neurosurgery, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK. E-mail adk4z{at}clinmed.gla.ac.uk

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.


Key Words: amyloid • apolipoprotein • cerebrospinal fluid • subarachnoid hemorrhage




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