Linkage and Association Studies

In terms of the genetics of schizophrenia, additive and interactive genes are thought to increase the possibility of developing the disorder, although this outcome is not inevitable even with the requisite genetic combination. Linkage studies, which assess genetic factors within families, have suggested that mutations on chromosomes 6p, 8p and 11q are possible contributors to the development of the disorder [16-18]. Association studies offer another method for uncovering the genetic underpinnings of schizophrenia by looking at disease markers in unrelated persons or animals [19]. One example of an association study using an animal model comes from Joober et al. [20]. Using mouse genetics and quantitative trait locus (QTL) analysis, they explored mouse prepulse inhibition, which refers to ''an inhibition of the startle response when a low-intensity stimulus, the prepulse, preceded the startling stimulus (by 30-500 ms)'' [20]. Deficits in prepulse inhibition are associated with attentional problems and other cognitive deficits, both of which are observed in persons with schizophrenia [21]. Based on this work, Joober and colleagues have uncovered two candidate genes in mice, which may be related to sensorimotor gating deficits in humans [20]. With the mapping of the human genome, future breakthroughs in understanding the aetiology of schizophrenia are surely on the horizon. Deciding how to apply this information in a useful and ethical manner remains a continuing area of debate, one that will be addressed briefly later in this chapter.

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