Specific learning disorder (SLD) is a neurodevelopmental disorder that significantly affects children’s academic performance. This study aimed to investigate the expression levels of the MAP Kinase Interacting Serine/Threonine Kinase 1–2 ( MNK1 , MNK2 ), Synaptic Ras GTPase Activating Protein 1 ( SYNGAP1 ) genes, and the long non-coding RNA Synaptic Ras GTPase Activating Protein 1-Anti Sense1 ( SYNGAP1-AS1 ), which are believed to play a key role in neurodevelopmental pathways, in children with SLD. Understanding the role of these genes in synaptic plasticity and cognitive function may provide insights into the molecular mechanisms underlying SLD. This study included 38 children diagnosed with SLD and 35 healthy controls aged 6 to 16. RNA was isolated from blood samples, and gene expression levels were measured using quantitative polymerase chain reaction (qPCR). The statistical analysis was conducted to compare the expression levels between the SLD and control groups and within SLD subgroups based on severity and sex. MNK1 and SYNGAP1 expression levels were significantly upregulated in the SLD group compared to the control group (8.33-fold and 16.52-fold increase, respectively; p < 0.001). lncSYNGAP1-AS1 showed a 26.58-fold increase, while MNK2 was downregulated by 2.2-fold, although these changes were not statistically significant. No significant differences were observed between sexes or between the severity subgroups of SLD. Conclusion : he upregulation of MNK1 and SYNGAP1 in children with SLD suggests their involvement in the neurodevelopmental pathways associated with cognitive processes such as learning and memory. These findings provide a foundation for future research into the molecular basis and potential therapeutic targets of SLD. What is known: • SYNGAP1 is a key regulator of synaptic plasticity and learning, primarily functioning through Ras signaling inhibition. Its deficiency impairs long-term potentiation (LTP) and is associated with neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD) and intellectual disability. • The MAPK/ERK pathway plays a crucial role in learning and memory, and its dysregulation has been linked to several neurological conditions. MNK1/2 interacts with SYNGAP1 in synaptic signaling. What is new: • This study is the first to demonstrate significant upregulation of SYNGAP1 and MKNK1 in children with SLD. • Understanding the role of the MKNK-SYNGAP1 axis may guide the development of targeted therapies aimed at enhancing synaptic plasticity to improve learning and memory outcomes in children with SLD.

Coronary artery disease (CAD) is the leading cause of fatalities worldwide. Nuclear factor (NF)-κB is a transcription factor that controls cell proliferation, differentiation and immunity. To the best of our knowledge, the present study is the first investigation of the association between CAD and NF-κB1 −94 W/D/NF-κBIA 3′-untranslated region (3′-UTR) A→G polymorphisms. The study population comprised 226 CAD patients and 201 controls. There was no significant difference in NF-κB1A 3′-UTR A→G in the allele and genotype frequencies between case and control populations. The D allele frequency of NF-κB1 −94 in the case group was significantly higher compared to the control group (P=0.028, odds ratio=1.37). The genotype frequency of NF-κB1 −94 DD in the case group was significantly higher compared to the controls (P=0.028). Linkage analysis showed a close linkage among these 2 genes (P<0.001 for case and control), and AD and GD haplotypes were associated with CAD (P<0.001; P=0.015, respectively). NF-κB1 −94 DD genotype can be a significant risk factor for the development of CAD.

Specific learning disorders (SLD) are neurodevelopmental disorders that affect cognitive abilities such as reading, writing, and mathematics. The molecular mechanisms underlying SLD remain unclear, though genetic and epigenetic factors are thought to play a significant role. MeCP2 is an epigenetic regulator that binds to methylated DNA, playing a crucial role in the regulation of gene expression and SP in neuronal cells. PTEN, a tumor suppressor gene, regulates cell growth, survival, and apoptosis, and is critical for maintaining synaptic integrity. In this study, we aimed to examine the expression of MeCP2 and PTEN in individuals with SLD. RNA was isolated from blood samples, and gene expression was assessed using quantitative PCR (qPCR). A total of 38 participants with SLD and 35 healthy controls were included in the study. Our results revealed a 15.44-fold upregulation of MeCP2 and a 13.66-fold downregulation of PTEN in the SLD group compared to controls, suggesting a disrupted balance of gene expression. There was no significant difference in gene expression between severe and non-severe SLD groups. These findings suggest that the dysregulation of MeCP2 and PTEN may be involved in the pathophysiology of SLD, influencing SP and neuronal function. In conclusion, the altered expression of these genes in individuals with SLD highlights potential biomarkers for early diagnosis and therapeutic targets, opening avenues for future research and intervention strategies.