Molecular genetics

For almost 15 years researchers have been using molecular techniques to seek the gene or genes that predispose to schizophrenia. The first technique to be used was that of linkage in which large families with several members affected with schizophrenia are studied to try and find a genetic marker that cosegregates with the disease. Unfortunately, to date no single gene or indeed region has been unequivocally implicated in susceptibility to schizophrenia. Rather, linkage studies suggest that no gene can exist which increases the risk of schizophrenia by more than a factor of 3 but that there may be a number of susceptibility genes. Recent findings suggest that some of these may lie within 'hot spots' on chromosomes 22, 6, or 13 (reviewed by Kirov and Murray(11,).

The second approach, that of association studies, takes a gene that is suspected of involvement in the pathogensis of the disorder (e.g. a gene involved in dopamine metabolism) and then compares the frequency of its various alleles in a series of individuals with schizophrenia as opposed to a control group. Some candidate gene studies imply a weak effect of the D3 dopamine and 5-HT2A receptor genes as well as the HLA locus on chromosome 6.(12)

Other studies have noted that patients in successive generations tend to develop frank schizophrenia at ever earlier ages. This process of 'anticipation' occurs in a number of neurological conditions in which an excess number of trinucleotide repeats occurs, and increases with succeeding generations; some claim that the same occurs in schizophrenia but most studies do not (see Kirov and Murray(11)).

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