Glial fibrillary acidic protein: a potential blood biomarker for acute ischemic stroke

Abstract Background Thrombosis and embolism of cerebral arteries cause reduced blood flow and oxygen supply to the brain, resulting in neuronal damage and astrocyte activation, which leads to the release of glial fibrillary acidic protein (GFAP) into cerebrospinal fluid and blood. In this single-center case–control study we evaluated serum glial fibrillary acidic protein (GFAP) levels in patients with acute ischemic stroke and matched healthy controls and assessed associations with stroke severity and 3-month functional outcome. Results Mean GFAP serum level was significantly higher in cases (0.206 ± 0.097 ng/mL) than controls (0.068 ± 0.058 ng/mL, p < 0.001). GFAP correlated positively with NIHSS on day 1 (r = 0.443, p = 0.027) and day 7 (r = 0.654, p < 0.001) and with mRS at 3 months (r = 0.632, p = 0.001). ROC analysis for discriminating acute ischemic stroke from healthy controls gave AUC 0.886 (95% CI 0.790–0.982); at a cutoff of 0.15 ng/mL sensitivity was 76.0% (95% CI 54.9–90.6) and specificity 88.0% (95% CI 68.8–97.5). Post-hoc power for the observed case–control difference in means was > 99% (Cohen’s d = 1.73). Conclusion Serum GFAP levels are significantly elevated in acute ischemic stroke and correlate with stroke severity and functional outcome, providing preliminary evidence supporting further investigation of GFAP as a potential prognostic biomarker.