ABSTRACT
In the early 1990s, when the neuropsychological component of the Maudsley Family Study of Psychosis (MFSP) began, it was thought that genes modulating cognitive function might partially overlap with those that increase liability to schizophrenia. This is not a surprising idea given that schizophrenia manifests itself, through its symptoms, to some extent at the cognition level. However, for a long time the de®cits seen in cognition were viewed as a result of the disease, rather than being part of the mechanism that gives rise to it. The shift in thinking occurred for some following a number of reports. First, there were studies suggesting that cognitive impairment is present not only in patients with chronic schizophrenia but even in those who experience their ®rst episode (Gur et al., 1991; Saykin et al., 1991), implying that the cognitive de®cit seen in patients with schizophrenia is not only a result of chronic illness. Similarly, reports of cognitive de®cits among unmedicated patients (Saykin et al., 1994) meant that researchers could no longer dismiss cognitive impairment as a consequence of medication usage. Furthermore, longitudinal studies showed that the cognitive de®cits remain relatively stable throughout the course of illness (Censits et al., 1997; Rund, 1998), reinforcing the idea that the cognitive impairment is a stable trait that does not disappear when the symptoms fade away. Finally, ®ndings of cognitive abnormalities in pre-schizophrenic children or adults (David et al., 1995; Jones et al., 1994) indicated that the
impairment predates the onset of psychosis, and cannot simply be an epiphenomenon of the disease process.
