The present findings of abnormal gamma-band responses in CHR patients that are intermediate between young schizophrenia patients and healthy controls indicate that these abnormalities predate psychosis onset, at least in a subset of a CHR patients. While the pathophysiological mechanisms giving rise to these gamma band abnormalities remain to be elucidated, it is reasonable to hypothesize that these mechanisms involve dysfunction of the GABAergic and NMDA glutamatergic micro-circuitry known to subserve gamma oscillations (Carlen et al., 2011; Sohal et al., 2009) that have already been implicated in the pathophysiology of schizophrenia (Benes, 2000; Doheny et al., 2000; Gonzalez-Burgos and Lewis, 2008; Gonzalez-Burgos et al., 2010; Hashimoto et al., 2003; Lewis et al., 2005; Lewis et al., 2011; Lewis et al., 2008; Roopun et al., 2008). In line with previous studies reporting impaired GBR measures in unaffected siblings (Leicht et al., 2010a) and unaffected co-twins of schizophrenia patients (Hall et al., 2011b), the current findings suggest that abnormal early auditory gamma-band response may be a biomarker reflecting the clinical risk for the development of psychosis. However, we did not find abnormal
