rendering these unbiased measures suitable tools to study interindividual differences in olfactory processing. This is a necessary prerequisite for ongoing efforts for identifying endophenotypes for schizophrenia, which may aid an early intervention before the onset of psychosis (e.g., Corcoran et al., 2010; Fusar-Poli et al., 2012b). Although one may invoke the often suspected limitations of the surface Laplacian (see Tenke & Kayser, 2012, p. 2342) as a cause of attenuated group differences, there is no empirical basis for this argument for the present data (see supplementary Figures S1–S4). Despite the absence of overall group differences in nasal chemosensory performance or olfactory N1 and P2 amplitudes, the present results imply a greater variability of odor processing among high-risk individuals and thereby contribute to the growing evidence showing pre-psychosis abnormalities of olfactory function in schizophrenia, which merits further research in a larger sample employing either a cross-sectional (e.g., including CHR, first-episode, and chronic schizophrenia patients) or a longitudinal design with more comprehensive measures of olfactory processing.
