Background: Alzheimer disease (AD) is a typical progressive and destructive neurodegenerative disease that has been studied extensively. However, genetic features and molecular mechanisms underlying AD remain unclear. Here we used bioinformatics to investigate the candidate nuclear genes involved in the molecular mechanisms of AD. Material/Methods: First, we used Gene Expression Omnibus (GEO) database to obtain the expression profiles of the mRNAs from hippocampus microarray and identify differentially expressed genes (DEGs) the plier algorithm. Second, functional annotation and visualization of the DEGs were conducted by the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Finally, BioGRID, IntAct, STRING, and Cytoscape were utilized to construct a protein-protein interaction (PPI) network. Hub genes were analytically obtained from the PPI network and the microRNA (miRNA)-target network. Results: Two hippocampus microarrays (GSE5281 and GSE48350) were obtained from the GEO database, comprising 161 and 253 cases separately. Among these, 118 upregulated genes and 694 downregulated genes were identified. The upregulated DEGs were mainly involved in positive regulation of transcription from RNA polymerase II promoter, positive regulation of cartilage development, and response to wounding. The downregulated DEGs were enriched in chemical synaptic transmission, neurotransmitter secretion, and learning. By combining the results of PPI and miRNA-target network, 8 genes and 2 hub miRNAs were identified, including YWHAZ, DLG4, AGAP2, EGFR, TGFBR3, PSD3, RDX, BRWD1, and hsa-miR-106b-5p and hsa-miR-93-5p. These target genes are highly enriched in various key pathways, such as amyloid-beta formation, regulation of cardiocyte differentiation, and actin cytoskeleton reorganization. Conclusions: In this study, YWHAZ, DLG4, AGAP2, EGFR, TGFBR3, PSD3, RDX, and BRWD1 were identified as candidate genes for future molecular studies in AD, which is expected to improve our understanding of its cause and potential molecular mechanisms. Nuclear genes, DEGs, and related networks identified by integrated bioinformatics analysis may serve as diagnostic and therapeutic targets for AD.

Background The combined effects of bilateral corticospinal tract (CST) reorganization and interhemispheric functional connectivity (FC) reorganization on motor recovery of upper and lower limbs after stroke remain unknown. Material/Methods A total of 34 patients underwent magnetic resonance imaging (MRI) examination at weeks 1, 4, and 12 after stroke, with a control group of 34 healthy subjects receiving 1 MRI examination. Interhemispheric FC in the somatomotor network (SMN) was calculated using the resting-state functional MRI (rs-fMRI). Fractional anisotropy (FA) of bilateral CST was recorded as a measure of reorganization obtained from diffusion tensor imaging (DTI). After intergroup comparisons, multiple linear regression analysis was used to explore the effects of altered FA and interhemispheric FC on motor recovery. Results Interhemispheric FC restoration mostly occurred within 4 weeks after stroke, and FA in ipsilesional remained CST consistently elevated within 12 weeks. Multivariate linear regression analysis showed that the increase in both interhemispheric FC and ipsilesional CST-FA were significantly correlated with greater motor recovery from week 1 to week 4 following stroke. Moreover, only increased FA of ipsilesional CST was significantly correlated with greater motor recovery during weeks 4 to 12 after stroke compared to interhemispheric FC. Conclusions Our results show dynamic structural and functional reorganizations following motor stroke, and structure reorganization may be more related to motor recovery at the late subacute phase. These results may play a role in guiding neurological rehabilitation.

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