The paradox of an ever increasing volume of research data, and the apparent stalemate of the search for causes of the disorder, has fuelled doubts about the validity of the schizophrenia construct, some leading to proposals to discard the category 7, 8 or to replace it with a pre-Kraepelinian notion of a unitary ‘psychosis’. 4, 5, 6 Thus, the existence of a specific brain disease underlying schizophrenia is still a hypothesis, for which no conclusive proof or refutation has yet been produced. Genetic linkage and association studies have targeted multiple candidate loci and genes, but failed to demonstrate that any specific gene variant, or a combination of genes, is either necessary or sufficient to cause schizophrenia. Yet none of these variables has to date been definitively proven to possess the sensitivity and specificity expected of a diagnostic test. Research has marked out numerous biological indicators tentatively associated with the disorder, including neurocognitive dysfunction, brain dysmorphology, and neurochemical abnormalities. Despite the availability of criteria 2, 3 allowing reliable diagnostic identification, schizophrenia essentially represents a broad clinical entity defined by subjective symptoms, behavioural signs, and patterns of course. More than a century since the delineation of dementia praecox by Kraepelin, 1 the aetiology, neuropathology, and pathophysiology of schizophrenia remain elusive.