## 3 Results and Discussion
MF analysis showed enrichment in cadherin binding, with these proteins' participation in the development and functional organization of the adult neural tissue, axon elongation and synaptogenesis [33]. The ribosomal protein L11 (_RPL11_) was also detected, which encodes RPL11. In a recent study, RPL11 was detected in the brain cerebral gray and white matter of AD and control donors [34]. Regarding _TGFBR3_, increased levels of this gene have been observed through functional genomic analysis in the temporal cortex of AD patients and particularly, its promoter methylation level was downregulated and negatively related to the AB level. The promoter hypomethylulation of the gene in A\(\beta\) accumulation has been executed through the enhancement of \(\beta\)- and \(\gamma\)-secretase activities, while mediators of the synaptic vesicle cycle, calcium signaling pathway and glutamatergic synapse pathways are associated with an expressed protein [35]. Ras Homolog Family Member C (_RhoC_), another high-scored gene in our analysis, encodes a member of the Rho family of small GTPases, which are involved in the reorganization of actin cytoskeleton while their expression of some members of this family has been linked with the diminution of human brain malignancy [36]. This was verified through pathways enrichment analysis according to Table S6, which shows mainly Rho GTPases activation pathways as well as semaphorin interactions and sema4D-induced cell migration. In neural stem/progenitor cells, the expression of _RhoC_ was down regulated by  
Figure 3: GO term and pathway enrichment analysis performed using Enrichr on DEGs. (**A**) The top 10 enriched Reactome pathway for DEGs. (**B**) The top 10 enriched biological processes for DEGs. (**C**) The top 10 enriched molecular functions for DEGs. (**D**) The top 10 enriched cellular components for DEGs. the presence of A\(\beta\)42, demonstrating its contribution to the migration of these cellular types as a sufficient indicator for NSFCs' migration capacity [37]. GO analysis demonstrated that _RloC_ in BP was significantly enriched in the regulation of lipase activity, cortical cytoskeleton organization and mitotic cytokinesis in MF with GTP and guanyl ribonucleotide binding and in CC with neuron projection, cytoskeleton and intracellular membrane and non-membrane-bounded organelles (Tables S7-S9). _LMNA_ encodes lamin A/C: a two-dimensional matrix of proteins located next to the inner nuclear membrane, which is both made from the _LMNA_ gene through alternative splicing. Deficiencies in A-type lamins account for cardiomyopathy, muscular dystrophy, peripheral neuropathy and progeroid disorders, even if the significance of lamin A in the brain is not clear, probably because A-type lamins are expressed at later stages when cells undergo differentiation. According to previous studies, the expression of lamin A may depend on the epigenetic regulation of LMNA. However, it should be stressed that the adult brain preferentially expresses C-type lamin rather than type-A lamin [38]. Although gene mutations have been related to an increasing number of diseases, often involving skeletal and cardiac muscle, [PERSON] et al. indicated a correlation of the gene with patients affected by the neuromuscular disease [39]. Pathways enrichment analysis showed that _LMNA_ was mainly enriched in the depolymerization of the nuclear lamina, deregulated CDK5 neurodegenerative pathways in AD models, and the defective intrinsic pathway for apoptosis and meiotic synapsis, while BP showed enrichment in the regulation of cell aging and mitotic nuclear membrane organization and reassembly (Tables S10 and S11). Fc Epsilon Receptor Ig (_FCERIG_), another observed high score gene, was expressed in dissociated mouse dorsal root ganglia neurons, but the function of the neuronal protein was unknown. [PERSON] et al. showed the significant upregulation of the protein in small-sized trigeminal ganglion neurons in the ovalbumin-sensitized mouse model [40].