PMC:4182838 / 1708-6070
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4182838","sourcedb":"PMC","sourceid":"4182838","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4182838","text":"Background\n22q11.2 deletion syndrome (22q11DS) is caused by a deletion on the long arm of chromosome 22 and is thought to affect between 30 and 60 genes associated with brain development and function [1]. Our ability to function and thrive in life is reliant on our capacity to select and attend to salient information in our environment and to ignore or inhibit non-salient information. The impairment of inhibitory information processes is associated with a wide range of psychiatric illnesses [2], including those common to 22q11DS such as schizophrenia. People with 22q11DS are at a greater risk of developing schizophrenia and other psychotic disorders [3–5], and genome-wide association studies (GWAS) indicate that the 22q11.2 deletion represents the strongest known genetic association in schizophrenia [1, 6]. Compared to control participants, people with schizophrenia as well as their first-degree relatives show poorer performance on inhibitory information processing measures of pre-pulse inhibition [PPI; [7–10]] and antisaccade inhibition [11, 12]. There is also evidence to suggest that pre-pulse inhibition is similarly impaired in 22q11DS [13, 14]. Inhibitory dysfunction observed prior to the onset of schizophrenia in groups at a genetic high risk for the disorder suggests that inhibitory dysfunction may represent a trait marker for developing schizophrenia [10]. Moreover, information processing difficulties may also account for some of the higher-order cognitive impairments that are commonly reported in 22q11DS such as executive dysfunction [15].\nPPI is a measure of reduction of the acoustic startle response when a weak non-startling stimulus (pre-pulse; S2) is presented before a startling stimulus (S1) [16] and reflects pre-attentive and automatic sensorimotor gating mechanisms [17]. Reduced PPI has been consistently reported in people with schizophrenia [7, 9, 18], and it is considered a potential endophenotype for the disorder [9]. In healthy controls, typical levels of PPI are between 50% and 60% (though levels are influenced by factors such as stimulus type (e.g. white noise/pure tone) and interstimulus interval (ISI)) [18]. However, when variations of this paradigm include both attended and unattended conditions, individuals with schizophrenia show deficits in PPI only when instructed to attend to the pre-pulse [19, 20]. While reduced PPI is reported using unattended measures of PPI alone, it is not known whether impaired attention modulation of PPI is similarly observed in 22q11DS as in schizophrenia.\nThe antisaccade paradigm is another measure of inhibitory information processing and requires the participant to suppress a saccade to a stimulus (prosaccade) and generate a saccade to the mirror position (antisaccade) [21]. It is a voluntary executive control process regulated strongly by prefrontal cortical areas; however, both early pre-attentional or automatic and later controlled attentional processes contribute to generating the antisaccade [22]. In healthy controls, antisaccade error rate is estimated at 20% [23], and in schizophrenia, antisaccade error rate is significantly and consistently higher and is associated with poor executive functioning [24–26]. Despite evidence of poor executive functioning in 22q11DS [15, 27] and evidence linking antisaccade impairment to a locus on chromosome 22q11-12 [28], antisaccade performance has not been examined in 22q11DS.\nThe present study sought to extend previous inhibitory information processing studies in 22q11DS by examining attended and unattended measures of PPI, antisaccade inhibition and associations with executive functioning prior to the onset of overt psychosis. Consistent with previous studies [14], we expect to report reduced unattended PPI in participants with 22q11DS. Given evidence of attention deficits in 22q11DS, it is expected that when instructed to attend to the pre-pulse, compared to typically developing control participants, the 22q11DS group will fail to show normal attentional modulation of the startle response. In addition, we expect to show increased antisaccade error rates in the 22q11DS group compared to typically developing controls and that poorer antisaccade performance will be associated with poorer performance on attention-dependent neuropsychological tasks (executive functioning) in both 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