Genetic models

Thus, both statistical and molecular studies indicate that schizophrenia cannot be explained by the inheritance of a single major gene. In any case, such simple Mendelian inheritance would be hard to square with the persistence of schizophrenia in the population. Since people with schizophrenia tend to reproduce less frequently than the rest of the population, one would have expected that a single major gene with such damaging consequences would have been selected out of the gene pool.

The evidence is compatible with oligogenic inheritance (a small number of genes involved) but the most popular model is the polygenic model which postulates that a number of genes of small effect are involved. Further support for this model comes from the fact that the risk to an individual increases with the number of affected relatives(1) and also with the finding of Cardno et al.(6) that the monozygotic concordance rate is higher for those twins who had an early rather than late onset of psychosis.

Family studies also show that the relatives of probands with an early onset have a higher morbid risk of psychosis than the relatives of late-onset patients. (1.3) These findings are compatible with the idea that schizophrenia is in part a developmental disorder and that some of the susceptibility genes may be involved in the control of neurodevelopment. (1i>

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