Globally across the brain, there were 109 DEGs uniquely normalized in response to hNSCs (i.e., not downregulated by IS), several known to be key in AD risk and pathogenesis, such as Trem2 (Keren-Shaul et al., 2017; Scheltens et al., 2021), Tyrobp (Pottier et al., 2016), S100a1 (Afanador et al., 2014; Cristóvão and Gomes, 2019), Igfbp5 (Barucker et al., 2015; Yu et al., 2018), Gfap (Benedet et al., 2021), and several complement genes (C1qa, C1qb, C1qc). This evidence concerns the gene C1QB and Alzheimer disease.