Specific Learning Disability (SLD) describes persistent difficulties in academic skills in reading, writing, and mathematics, despite having normal intelligence. The exact origin of SLD is unknown. However, it is thought that biological factors and environmental conditions, along with genetic factors, contribute to the development of SLD. Agmatine, a neurotransmitter in the brain, plays a role in various biological processes. Agmatine has been reported to mediate antidepressant effects and neuroprotective effects, and it plays critical roles in learning and the processing of learned information into memory. Therefore, this study aimed to determine the relationship between SLD and agmatine metabolism by determining the enzyme levels of arginine decarboxylase (ADC) and agmatinase (AGMAT) in children with SLD. ADC and AGMAT levels in the blood serum of children with SLD and controls were analyzed using ELISA. When ADC levels in children with SLD (30.26 ± 5.06 ng/mL) were compared with those in the control group (29.82 ± 4.95 ng/mL), the difference was not statistically significant (p = 0.737). However, AGMAT levels in children with SLD (27.02 ± 4.46 ng/mL) were found to be statistically significantly higher than those in the control group (21.42 ± 3.98 ng/mL) (p < 0.001). In light of these findings, we can say that agmatine breakdown is significantly increased in children with SLD.

Oxidative stress and apoptosis contribute to seizure-associated neuronal injury, but the effects of ML-171, a pharmacological NOX-1 inhibitor, on PTZ-associated oxidative and apoptotic injury remain insufficiently defined. This study evaluated the effects of the NOX-1 inhibitor ML-171 in pentylenetetrazole (PTZ)-induced cellular and animal models of neuronal injury. SH-SY5Y cells were exposed to PTZ (30 mM, 24 h) after pretreatment with ML-171 or valproic acid (VPA), and cell viability, redox status, apoptosis-related proteins, and Annexin V-based cell death were assessed. Adult male Wistar Albino rats were subjected to PTZ kindling and acutely treated with VPA or ML-171 (0.1, 1, or 10 mg/kg); behavioral seizures, electrocorticographic activity, hippocampal oxidative stress, apoptotic markers, histopathology, and NOX-1 immunoreactivity were evaluated. ML-171 attenuated PTZ-induced cellular injury in SH-SY5Y cells within a restricted concentration window and reduced oxidant burden, oxidative stress index, and apoptotic signaling. In PTZ-kindled rats, ML-171 improved hippocampal oxidative and apoptotic markers but did not robustly suppress behavioral or electrophysiological seizure parameters. Histopathological injury and NOX-1 immunoreactivity showed region- and dose-dependent responses. These findings suggest that ML-171 primarily attenuates PTZ-associated oxidative and apoptotic injury rather than exerting a conventional antiseizure effect.