Schizophrenia is a uniquely human disorder, whose phylogenetic appearance parallels that of glial evolution, which accelerated with the appearance of hominids (Horrobin, 1998; Oberheim et al., 2006; Oberheim et al., 2009). In particular, astroglial complexity and pleomorphism increased significantly with hominid evolution, which suggests an association between human glial evolution and the development of human-selective neurological disorders, the neuropsychiatric disorders as a case in point. Indeed, a number of both genome-wide association and differential expression studies have highlighted the frequent dysregulation of glial-selective genes, both astrocytic and oligodendrocytic, in schizophrenia (Aberg et al., 2006; Georgieva et al., 2006; Hakak et al., 2001; Hof et al., 2002; Roy et al., 2007; Takahashi et al., 2011; Walsh et al., 2008). At the same time, a number of investigators have highlighted the marked differences between humans and rodents in glial gene expression, in contrast to the relatively conserved nature of neuronal gene expression across mammals (Miller et al., 2010; Sim et al., 2009; Zhang et al., 2016). Together these studies suggest the correlative association of human glial evolution with the phylogenetic appearance of schizophrenia.
