http://nova.newcastle.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:241 A novel phenotyping strategy in schizophrenia, targeting different neurocognitive domains, neurobehavioral features, and selected personality traits, has allowed us to identify a homogeneous familial subtype of the disease, characterized by pervasive neurocognitive deficit. Our genome scan data indicate that this subtype, which accounts for up to 50% of our sample, has a distinct genetic basis and explains linkage to chromosome 6p24 reported previously. If representative of other populations, the ratio of schizophrenia subtypes observed in our families could have a profound impact on sample heterogeneity and on the power of genetic studies to detect linkage and association. Our proposed abbreviated battery of tests should facilitate phenotype characterization for future genetic analyses and allow a focus on a crisply defined schizophrenia subtype, thus promoting a more informed search for susceptibility genes. © 2005 by The American Society of Human Genetics. All rights reserved. 2012-03-01T02:36:05.204Z ]]> http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:97 Introduction. The frequency of auditory hallucinations (AH) is associated with efficiency in inhibiting irrelevant memories, suggesting that the presence of AH may be related to the intrusion of strongly activated representations in memory. Therefore, we hypothesised that the inability to suppress irrelevant memories would be found only in patients currently experiencing AH. Method. Performance on a repeated, continuous recognition task was examined in 23 schizophrenia patients with AH present, 20 schizophrenia patients with AH absent, and 24 healthy controls. Results. Patients with current AH made significantly more inappropriate responses (false alarms) to distractors seen on previous runs of the task than nonhallucinating patients. The ability to detect targets (hits) was significantly better in healthy controls than schizophrenia patients, however, there was no significant difference between the two patient subgroups. Conclusions. The findings confirm that the presence of AH involves a failure to suppress memories that are not relevant to ongoing reality. We propose that a combination of deficits in inhibition and (episodic) memory provides a useful model of AH, which can accommodate many of the characteristic features of the symptom and fits well with the neuroanatomical circuitry that is believed to underlie the occurrence of AH. 2010-04-27T05:35:45.714Z ]]>