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%O Copyright © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
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%D 2018
%J BMC Neurology
%T Transient increase in CSF GAP-43 concentration after ischemic stroke
%A A Sandelius
%A NC Cullen
%A A Kallen
%A L Rosengren
%A C Jensen
%A V Kostanjevecki
%A M Vandijck
%A H Zetterberg
%A K Blennow
%X Background: Cerebrospinal fluid (CSF) biomarkers reflect ongoing processes in the brain. Growth-associated
protein 43 (GAP-43) is highly upregulated in brain tissue shortly after experimental ischemia suggesting the CSF
GAP-43 concentration may be altered in ischemic brain disorders. CSF GAP-43 concentration is elevated in
Alzheimer’s disease patients; however, patients suffering from stroke have not been studied previously.
Methods: The concentration of GAP-43 was measured in longitudinal CSF samples from 28 stroke patients
prospectively collected on days 0–1, 2–4, 7–9, 3 weeks, and 3–5 months after ischemia and cross-sectionally in 19
controls. The stroke patients were clinically evaluated using a stroke severity score system. The extent of the brain
lesion, including injury size and degrees of white matter lesions and atrophy were evaluated by CT and magnetic
resonance imaging.
Results: Increased GAP-43 concentration was detected from day 7–9 to 3 weeks after stroke, compared to day 1–4
and to levels in the control group (P = 0.02 and P = 0.007). At 3–5 months after stroke GAP-43 returned to admission
levels. The initial increase in GAP-43 during the nine first days was associated to stroke severity, the degree of white
matter lesions and atrophy and correlated positively with infarct size (rs = 0.65, P = 0.001).
Conclusions: The transient increase of CSF GAP-43 is important to take into account when used as a biomarker for
other neurodegenerative diseases such as Alzheimer’s disease. Furthermore, GAP-43 may be a marker of neuronal
responses after stroke and additional studies confirming the potential of CSF GAP-43 to reflect severity and
outcome of stroke in larger cohorts are warranted.
%K GAP-43, Stroke, Neurodegeneration, Cerebrospinal fluid, Biomarkers
%I BMC
%L discovery10065062