@article{discovery10065062,
           month = {December},
           title = {Transient increase in CSF GAP-43 concentration after ischemic stroke},
          volume = {18},
            note = {Copyright {\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
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.},
       publisher = {BMC},
            year = {2018},
         journal = {BMC Neurology},
             url = {http://doi.org/10.1186/s12883-018-1210-5},
            issn = {1471-2377},
        keywords = {GAP-43, Stroke, Neurodegeneration, Cerebrospinal fluid, Biomarkers},
        abstract = {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.},
          author = {Sandelius, A and Cullen, NC and Kallen, A and Rosengren, L and Jensen, C and Kostanjevecki, V and Vandijck, M and Zetterberg, H and Blennow, K}
}