One of the most important and consistent findings that emerged from our transcriptomic profile was the enrichment of apoptotic genes in the DEGs. Aberrant apoptosis has been implicated in various neurodevelopmental and neurodegenerative disorders, including SZ [108–112]. Increased susceptibility to apoptosis in SZ patients may be responsible for synaptic/dendritic loss [113]. Reduced neuronal and glial viability, and volumetric and functional brain deficits observed in SZ are potentially associated with abnormal apoptosis [32]. Several studies have provided support to the hypothesis by showing increased brain Bax/Bcl-2 ratios and decreased levels of Bcl-2 and GSK3 [114–116]. In addition, a comprehensive integrated pathway analysis of GWAS and gene expression data also pointed to aberrant apoptosis as a potential cause of SZ [110]. In our study, we found similar evidence. Apoptotic genes such as Bak1 and BBC3 had significantly higher expression in SZ neurons, while GSK3A showed lower levels of expression. Two critical apoptotic factors, RBM5 and RBM6, also exhibited greater abundance in SZ neurons as well. Although statistically insignificant, CASP3 and CASP8 were also expressed at higher levels in the SZ samples. These
