## 3 Results
It is known to protect against neuronal death, as confirmed by animal model studies. Additionally, CNTF is upregulated following spinal cord injury and IS. In animal models, an astroglial upregulation of CNTF in the brain and CNTF expression in the hippocampus were observed for two weeks post-stroke. CNTF is recognized as a significant biomarker in various neurological diseases, including childhood IS. It directly impacts the nervous system by promoting neuron and oligodendrocyte survival, mediating neurogenesis, and exerting anti-inflammatory effects. Ciliary neurotrophic factor (CNTF) is reported to have a safe biological range, beyond which it may pose a risk of neurotoxicity. However, the dosing range appears sufficiently broad to minimize such risks. Improved functional outcomes have been observed following the administration of combined CNTF preparations via both oral and topical routes. In this study, the CNTF levels in the serum of patients with acute ischemic stroke were assessed, revealing a mean value of 7.84 \(\pm\) 0.322 pg/mL, with a wide range of variation (5.46 pg/mL to 20.26 pg/mL). In contrast, the control group showed a considerably narrower range of CNTF levels (4.94 pg/mL to 5.90 pg/mL) and a mean value of 5.29 \(\pm\) 0.067 pg/mL. This difference between the groups was statistically significant (\(p\) < 0.001) (Figure 5). Figure 4: Serum levels of VEGF in the acute period of childhood IS compared with the control group (pg/mL) [15]. A significant positive correlation was observed between the CNTF values in the main group (r = 0.72), compared to the control group (r = 0.208). The elevated CNTF levels in peripheral blood may reflect the concentration of this protein in the brain during IS, suggesting its potential role as a key biomarker of the disease. Notably, elevated CNTF levels are associated with significant neurotoxicity. However, during the progression of IS, CNTF levels below physiological thresholds may act as a neuroprotective factor, mitigating the pathological process in ischemic areas and preventing neuronal death, particularly in motor and sensory cells. The findings of the given study show that in this case, when CNTF levels exceeded the threshold for neurotoxicity, then neuroinflammationlammatory and neurodegenerative processes intensified. Early in the course of IS, reducing elevated CNTF levels through the administration of combined drugs--targeting pathways such as the CNTF-STAT3-IL-6 axis--may help to modulate the inflammatory cascade. The therapeutic regulation of CNTF levels in such cases represents a promising approach for preventing neurological complications, particularly in pediatric IS. Improved functional outcomes following the use of recombinant CNTF preparations have been widely documented in animal models. Additionally, this study analyzed other pro-inflammatory cytokines, including antiphospholipid antibodies (APAs), which act as vascular components and inflammatory markers. Elevated APA levels are associated with a hypercoagulable state, contributing to IS and other ischemic events. APAs, a heterogeneous group of autoantibodies, play a role in thrombosis through mechanisms such as the activation of coagulation cascades, ultimately leading to cerebral ischemia. The study group exhibited a mean APA level of 1.37 \(\pm\) 0.046 U/mL, significantly higher than the control group's mean level of 0.92 \(\pm\) 0.021 U/mL, activating coagulation cascades, causing cerebral ischemia. The figures reflect the APA values. Although the difference between the two groups may appear modest, a statistically significant disparity was observed (\(p\) < 0.001) (Figure 6). Molecular markers of inflammation are valuable tools for managing patients in the acute phase of ischemic stroke (IS), assessing their prognosis, and preventing neurologic complications. Interleukin-6 (IL-6) is a key inflammatory mediator, with elevated levels commonly observed in children with IS.