This risk varies according to the type of schizophrenia: the risk of becoming schizophrenic for a child of a hebephrenic or catatonic schizophrenic parent is 20.7% and 21.6%, respectively. This risk is decreased (10.4%)
for a child of a paranoid schizophrenic parent. Risk is also increased when more relatives are affected, for example, the morbid risk of directly schizophrenia for a child of two affected parents is 46%. The risk for other conditions is increased among relatives of schizophrenic Inhibitors,research,lifescience,medical patients. In particular, Kendler and Dieh9 have shown that the risk of schizotypal or paranoid personality disorders in relatives of schizotypal patients is four times that in control Inhibitors,research,lifescience,medical families. The risks of schizoaffective disorder, schizophreniform disorder, delusional disorders, and atypical psychosis are also significantly increased in the relatives of probands. Altogether, these data clearly demonstrate the existence of a family
concentration of schizophrenia. Twin studies provide an estimation of the importance of the genetic contribution. They have shown consistent evidence of a higher concordance for monozygotic (50%) than towards dizygotic (17%) twins10 and estimated the heritability for schizophrenia as close to 80%. 11 Gottesman and Bertelsen12 showed that Inhibitors,research,lifescience,medical rates of schizophrenia in offspring of identical twins discordant for schizophrenia were equal. These data suggest that individuals Inhibitors,research,lifescience,medical who possess the schizophrenia genotype do not necessarily express the disorder. Studies of twins clearly show that liability to schizophrenia is not completely genetic and is more likely a complex trait determined by several genes
interacting with the environment. Better knowledge of environmental risk factors may improve our ability to identify the genes for schizophrenia. In particular, there is now a reliable evidence that at least two environmental factors are involved in the etiology of schizophrenia: perinatal obstetric complications13 and prenatal Inhibitors,research,lifescience,medical viral infections, especially in the second trimester.14 No study has clearly answered the question of how the genetic risk interacts with environmental Cilengitide precipitants or is transmitted. However, the most consistent model of transmission is a multifactorial inheritance model with no major gene.15 Risch et al3 have also shown that data in schizophrenia are consistent with the existence of three to four loci interacting epistatically. It is very likely that when the number of loci increases, the risk alleles at these loci become very common in the population, of the order of 14% to 20%.16 Which chromosomal regions are the best candidates for containing schizophrenia susceptibility genes? Molecular genetic studies have so far failed to find any DNA variant that can be demonstrated to contribute to schizophrenia risk.