Background: Glial cell line–derived neurotrophic factor (GDNF), predominantly expressed by astrocytes, plays an important role in regulating microglial activation during hemorrhagic stroke. By modulating neuroinflammation, GDNF may protect against neurodegeneration and contribute to recovery through neuroplasticity. Aim: To evaluate the role of GDNF in the acute phase of hemorrhagic stroke and its potential as a biomarker for predicting clinical outcomes. Methods: A total of 83 patients with acute hemorrhagic stroke of various localizations were examined. Of these, 45 (54.2%) were men and 38 (45.7%) women, with a mean age of 62.3 years. All patients underwent standardized clinical and neurological assessment. Stroke severity and functional status were evaluated using the NIHSS, FOUR, Barthel Index, and Rankin scale, allowing classification into groups by disease severity. Results: In the control group, the mean GDNF level was 28.1 pg/ml. In patients with hemorrhagic stroke, GDNF levels measured within the first 3 hours were significantly elevated at 46.7 pg/ml (p<0.05 vs. control). By day 14, levels declined to 35.3 pg/ml (p<0.05 vs. control), and by day 30 further decreased to 32.1 pg/ml (p<0.05 vs. 3-hour values). Patients with an unfavorable course demonstrated either stable GDNF levels or a progressive decline during the acute phase. In contrast, patients with a favorable clinical course showed a relative increase in GDNF by day 14, suggesting activation of neuroprotective and neuroplastic mechanisms. Conclusions: Even in severe cases of hemorrhagic stroke, processes of neuroplasticity remain active in the long term. Dynamic changes in GDNF during the acute phase reflect underlying neuroinflammatory and neuroplastic responses of the brain. These findings suggest that GDNF may serve both as a biomarker for outcome prediction and as a potential therapeutic target in hemorrhagic stroke.
Rakhimbaeva et al. (2026) studied this question.