ArticleJournal of neurodevelopmental disorders2014
Pre-pulse inhibition and antisaccade performance indicate impaired attention modulation of cognitive inhibition in 22q11.2 deletion syndrome (22q11DS).
Article in Journal of neurodevelopmental disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The acoustic startle response in 22q11 deletion syndrome: from animal models to humans.Frontiers in neuroscience · 2025Review
- Reduced amplitude and slowed latency of the acoustic startle response in adolescents and adults with 22q11.2 deletion syndrome.Schizophrenia research · 2024Article
- Polymorphisms in CRYBB2 encoding βB2-crystallin are associated with antisaccade performance and memory function.Translational psychiatry · 2020Article
- Goal-Directed-Behavior in 22q11.2 Deletion Syndrome: Implication for Social Dysfunctions and the Emergence of Negative Symptoms.Frontiers in psychiatry · 2020Article
- Interrelationship Between Cognitive Control, Anxiety, and Restricted and Repetitive Behaviors in Children with 22q11.2 Deletion Syndrome.Autism research : official journal of the International Society for Autism Research · 2019Article
- Multimodal investigation of triple network connectivity in patients with 22q11DS and association with executive functions.Human brain mapping · 2017Article
- Visual perception and processing in children with 22q11.2 deletion syndrome: associations with social cognition measures of face identity and emotion recognition.Journal of neurodevelopmental disorders · 2016Article
- Developmental trajectories of executive functions in 22q11.2 deletion syndrome.Journal of neurodevelopmental disorders · 2016Article
- PRODH rs450046 and proline x COMT Val¹⁵⁸ Met interaction effects on intelligence and startle in adults with 22q11 deletion syndrome.Psychopharmacology · 2015Article
- Modeling a model: Mouse genetics, 22q11.2 Deletion Syndrome, and disorders of cortical circuit development.Progress in neurobiology · 2015Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background22q11.2 deletion syndrome (22q11DS) is associated with a number of physical anomalies and neuropsychological deficits including impairments in executive and sensorimotor function. It is estimated that 25% of children with 22q11DS will develop schizophrenia and other psychotic disorders later in life. Evidence of genetic transmission of information processing deficits in schizophrenia suggests performance in 22q11DS individuals will enhance understanding of the neurobiological and genetic substrates associated with information processing. In this report, we examine information processing in 22q11DS using measures of startle eyeblink modification and antisaccade inhibition to explore similarities with schizophrenia and associations with neurocognitive performance.
methodsStartle modification (passive and active tasks; 120- and 480-ms pre-pulse intervals) and antisaccade inhibition were measured in 25 individuals with genetically confirmed 22q11DS and 30 healthy control subjects.
resultsIndividuals with 22q11DS exhibited increased antisaccade error as well as some evidence (trend-level effect) of impaired sensorimotor gating during the active condition, suggesting a dysfunction in controlled attentional processing, rather than a pre-attentive dysfunction using this paradigm.
conclusionsThe findings from the present study show similarities with previous studies in clinical populations associated with 22q11DS such as schizophrenia that may indicate shared dysfunction of inhibition pathways in these groups.
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