Immunogenetics and schizophrenia

There is overwhelming evidence for a major contribution of genetic elements to the aetiology of schizophrenia (Slater & Cowie, 1971), but the principal problems remain; what is the nature of the hereditary contribution, and what is the path by which genetic information is translated into a frank behavioural disorder? The genetic evidence comes not only from the well-known family studies (0degaard, 1963; Elsasser, 1952;Schulz, 1932; Hallgren & Sjogren, 1959; Kay et al. 1975) and twin studies (Luxenburger, 1930; Essen-Moller, 1941; Kallmann, 1946; Slater, 1953;Tienari, 1968; Kringlen, 1968; Fischer et al. 1969; Gottesman & Shields, 1972), but also from the convincing cross-fostering and adoption studies (Heston, 1966; Kety et al. 1968; Mednick et al. 1974). From the latter, it seems clear that children with an affected biological parent have the same elevated chance of becoming ill, irrespective of whether they are reared by the natural parent or an adoptive or foster parent. That adoptive or foster homes are not themselves 'schizophrenogenic' is confirmed by the findings (Wender et al. 1971, 1974; Karlsson, 1974) that there is no increased incidence of schizophrenia in adopting parents or their other adopted children. In summary,