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Introduction. The majority of genetic studies into the psychoses over the last 2 decades have been predicated on the double assumption that (a) schizophrenia and bipolar

The majority of genetic studies into the psychoses over the last 2 decades have been predicated on the double assumption that (a) schizophrenia and bipolar disorder, as defined in Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV),¹ and International Statistical Classification of Diseases, 10th Revision ², are discrete, “natural” disease entities with distinct etiology and pathogenesis and (b) these disease entities can be identified by current operational diagnostic conventions, which are based on reported subjective symptoms and, to a lesser extent, on deteriorating performance of expected social roles. Data from genetic epidemiology have been called upon to justify the validity of this approach, often referred to as the “Kraepelinian dichotomy.”

It is important to note that this widely held notion is incorrect. Kraepelin's seminal work, which aggregated 3 previously described syndromes—hebephrenia, catatonia, and paranoid dementia—into the clinical entity of dementia praecox and delimited the latter from manic-depressive insanity, paranoia, and late paraphrenia introduced order in the previously chaotic field of nosology and laid down the foundation for the current classifications of psychotic disorders. It is not widely known that, in contrast to the narrowly defined manic-depressive psychosis, Kraepelin's dementia praecox was a broad clinical grouping, consisting of 9 clinical “forms,” also including what today would be termed schizoaffective disorder and mood-incongruent affective psychoses. However, in 1920, he wrote that “we cannot distinguish satisfactorily between these two illnesses and this brings home the suspicion that our formulation of the problem may be incorrect … the affective and schizophrenic forms of mental disorder do not represent the expression of particular pathological processes, but rather indicate the areas of our personality in which these processes unfold.”³

Thus, in his later years, Kraepelin continued to develop and refine his ideas about psychiatric diagnoses, and his thinking had in many ways moved on from the dichotomous classification by the end of his life. However, it is not the goal of this article to consider Kraepelin's views in relation to modern nosological practice. A discussion of this sort, although of historical interest, is not of direct relevance. Unfortunately, the dichotomous, categorical view of the psychoses has been reified in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, formulation (and its consequent versions), and most of the genetic, and other, research into psychoses has been based solely on the “given” diagnostic categories of schizophrenia and bipolar disorder as the phenotypes, notwithstanding the fact that their validity has been challenged by emerging data from many fields of psychiatric research.^4–6

In this article, we will first review the key pieces of evidence from genetic epidemiology that there is in fact a genetic overlap between the psychopathological entities that we currently refer to as bipolar disorder and schizophrenia. We will then review emerging evidence that the 2 diagnostic categories share specific susceptibility genes and that particular risk alleles may be associated with specific aspects of the phenotype.

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