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The commentaries on our target article, 'Psychosis and Autism as Diametrical Disorders of the Social Brain,' reflect the multidisciplinary yet highly fragmented state of current studies of human social cognition. Progress in our understanding of the human social brain must come from studies that integrate across diverse analytic levels, using conceptual frameworks grounded in evolutionary biology.

Crespi & Badcock (C&B) have presented a novel view that the influence of genomic imprinting causes diametrically opposite disorders: namely, psychoses and autism. I propose an extended hypothesis that while genomic imprinting is likely to have an influence on the pathogenesis of psychoses and autism, it might contribute to phenomenological antithesis between as well as within these disorders.

Crespi & Badcock (C&B) hypothesize that biases toward expression of paternally or maternally imprinted genes lead to the symptoms of autism spectrum disorders (ASD) and psychotic-spectrum disorders (PSD), respectively. We suggest that such genetic risk factors may act by inducing abnormalities in developmental and learning-related plasticity. We provide preliminary evidence of abnormal plasticity in ASD and suggest transcranial magnetic stimulation as a useful tool to investigate as well as influence cortical plasticity.

By conceiving of autism and psychosis as diametrically opposite phenotypes of underactive and overactive mentalizing, respectively, Crespi & Badcock (C&B) commit themselves to a continuum view of intercorrelated mentalizing functions. This view fails to acknowledge dissociations between mentalizing functions and that psychotic people show a mixture of both hypo- and hyper-mentalizing.

In the target article, Crespi & Badcock (C&B) propose a novel hypothesis based on observations that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autism-spectrum versus psychotic-spectrum conditions. They propose that development of these conditions is mediated in part by alterations in 'genomic imprinting.' This hypothesis is based on the model of the Prader-Willi and Angelman syndromes. The authors have produced a masterful discussion of the 'differences between psychosis and autism. Of course, another article could be written on the similarities,