"Acquittal" for Suspected Schizophrenia Gene
Just under one per cent of all Germans suffer from schizophrenia. The susceptibility to contracting this severe psychological disease is inherited; various studies indicate that a gene on chromosome 1 shares responsibility for the outbreak of the disease. However, in what is the biggest control study to date, which is being published in the May edition of the prestigious scientific journal Science, the researchers conclude that the suspect gene plays a less important role than was expected. Centres of research in America, Australia and Europe are taking part, among them the University of Bonn’s Psychiatric Clinic.
Schizophrenia patients cannot distinguish between the imaginary and real worlds; they feel they are being persecuted, hear voices giving them orders, or see things which no-one else can see. The disease usually develops in phases; periods which are almost free of symptoms alternating with phases in which the delusions gain the upper hand. The medication currently available has unpleasant side-effects; the repercussions of the disease also extend to the patients’ social sphere.
The onset of schizophrenia frequently occurs in particular stress situations; the susceptibility, however, seems to be largely hereditary: if one of a pair of identical twins is schizophrenic, there is a 45% to 60% probability that the other one will also suffer from the disease. In many studies worldwide, scientists are attempting to identify the genes responsible for the outbreak of this severe psychological disease, so as to be able to develop more effective therapies. Until recently the hot favourite for the location of one of these genes was the 1q area on chromosome 1.
The scientists participating in the study have now investigated 779 families with 1918 schizophrenia patients to determine whether this hypothesis is true. In this they made use of the observation that genes which are adjacent to each other are frequently inherited together – this being all the more probable the smaller the spatial distance between them is. For example, if the father is the bearer of a gene which may trigger schizophrenia, whereas the mother is healthy, the DNS sequences surrounding the “schizophrenia gene” in the affected child are more likely to originate from the father – an effect which is known as “linkage”.
The researchers investigated the transmission of a total of 16 DNS sequences to chromosome 1q. None of these gene sequences is linked to schizophrenia in the families investigated. “We therefore assess the likelihood that the area on chromosome 1q is a major factor in the outbreak of schizophrenia as small,” Dr. Sibylle Schwab of the University of Bonn’s Clinic and Polyclinic for Psychiatry and Psychotherapy explains.
The study thereby contradicts the findings of Finnish, Canadian and Scottish teams which definitely do point to the involvement of chromosome 1q. However, in all three studies the number of patients studied was considerably less, so that a much smaller genetic heterogeneity can be assumed.
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