Background: Cerebrospinal fluid (CSF) biomarkers reflect ongoing processes in the brain. Growth-associated\nprotein 43 (GAP-43) is highly upregulated in brain tissue shortly after experimental ischemia suggesting the CSF\nGAP-43 concentration may be altered in ischemic brain disorders. CSF GAP-43 concentration is elevated in\nAlzheimerâ??s disease patients; however, patients suffering from stroke have not been studied previously.\nMethods: The concentration of GAP-43 was measured in longitudinal CSF samples from 28 stroke patients\nprospectively collected on days 0â??1, 2â??4, 7â??9, 3 weeks, and 3â??5 months after ischemia and cross-sectionally in 19\ncontrols. The stroke patients were clinically evaluated using a stroke severity score system. The extent of the brain\nlesion, including injury size and degrees of white matter lesions and atrophy were evaluated by CT and magnetic\nresonance imaging.\nResults: Increased GAP-43 concentration was detected from day 7â??9 to 3 weeks after stroke, compared to day 1â??4\nand to levels in the control group (P = 0.02 and P = 0.007). At 3â??5 months after stroke GAP-43 returned to admission\nlevels. The initial increase in GAP-43 during the nine first days was associated to stroke severity, the degree of white\nmatter lesions and atrophy and correlated positively with infarct size (rs = 0.65, P = 0.001).\nConclusions: The transient increase of CSF GAP-43 is important to take into account when used as a biomarker for\nother neurodegenerative diseases such as Alzheimerâ??s disease. Furthermore, GAP-43 may be a marker of neuronal\nresponses after stroke and additional studies confirming the potential of CSF GAP-43 to reflect severity and\noutcome of stroke in larger cohorts are warranted.
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