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In This Issue

In the review, Crow (pp. 1681–1685) examines current evidence on genetics and schizophrenia. He argues that findings to date have been disappointing, with initial findings on candidate genes being followed by a failure of replication in large sibling pair linkage surveys and targeted association studies. He further argues that the proposition that this failure to replicate indicates the existence of many susceptibility genes of relatively small effect approaches the unfalsifiable. The data, Crow argues, point to epigenetic processes, i.e. variation not in the DNA sequence but in transgenerational modification of the DNA sequence. Three commentaries assess the arguments made by Crow. In the first, Collier (pp. 1687–1691) comments that the polygene hypothesis is difficult to test, because of the required samples, but that this does not make it unfalsifiable. He further notes the importance of investigating gene x environment interactions. In the second commentary, Sullivan (pp. 1693–1696) argues that two of Crow’s conclusions are premature : (1) that genetic wide association studies will not work for schizophrenia, when GWAS has yielded significant findings for a range of other complex disorders ; and (2) that there is an epigenetic basis for schizophrenia, when there remain other plausible hypotheses to account for current data. In the final commentary, O’Donovan et al. (pp. 1697–1699) argue that there is strong (but not necessarily conclusive) support implicating some genes in schizophrenia (DTNBP1, NRG1, G72, DISC1). That the evidence is not yet absolutely conclusive, the authors argue, does not mean they are false-positive findings, but merely that some uncertainty remains.