Interestingly, we detected increased expression of GFAP, an astrocyte marker, decreased expression of MAP2, a neuronal marker, and elevated ratio of GFAP/MAP2, in postmortem brains of patients with schizophrenia. This may correspond to the aberrant neurogenic-to-gliogenic transition balance seen in the neurospheres derived from schizophrenia patients with the 22q11.2 deletion. Therefore, the theory of ‘reduced neurogenic and elevated gliogenic competences' could be a hallmark of schizophrenia pathology.48 With respect to a potential mechanism of elevated GFAP expression in the postmortem brains, several studies have reported that oxidative stress and inflammatory cytokines contribute to the pathophysiology of schizophrenia.49 However, in our postmortem brains, the examined inflammatory markers, IL1B and IL6, were not upregulated in the disease group nor did their expression levels correlate with GFAP levels. Therefore, upregulated GFAP expression is unlikely to be related to the inflammatory status at autopsy.
