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Schizophrenic‐like neurocognitive deficits in children and adolescents with 22q11 deletion syndrome
Author(s) -
Lewandowski Kathryn Eve,
Shashi Vandana,
Berry Peggy M.,
Kwapil Thomas R.
Publication year - 2006
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30379
Subject(s) - neurocognitive , psychology , schizophrenia (object oriented programming) , working memory , cognition , neuropsychology , executive functions , verbal memory , deletion syndrome , psychosis , cognitive remediation therapy , attention deficits , clinical psychology , developmental psychology , psychiatry , biochemistry , chemistry , gene , phenotype
22q11.2 Deletion Syndrome (22q11DS) is the most common genetic microdeletion syndrome affecting humans. The syndrome is associated with general cognitive impairments and specific deficits in visual‐spatial ability, non‐verbal reasoning, and planning skills. 22q11DS is also associated with behavioral and psychiatric abnormalities, including a markedly elevated risk for schizophrenia. Research findings indicate that people with schizophrenia, as well as those identified as schizoptypic, show specific cognitive deficits in the areas of sustained attention, executive functioning, and verbal working memory. The present study examined such schizophrenic‐like cognitive deficits in children and adolescents with 22q11DS (n = 26) and controls (n = 25) using a cross‐sectional design. As hypothesized, 22q11DS participants exhibited deficits in intelligence, achievement, sustained attention, executive functioning, and verbal working memory compared to controls. Furthermore, deficits in attention and executive functioning were more pronounced in the 22q11DS sample relative to general cognitive impairment. These findings suggest that the same pattern of neuropsychological impairment seen in patients with schizophrenia is present in non‐psychotic children identified as at‐risk for the development of schizophrenia based on a known genetic risk marker. © 2006 Wiley‐Liss, Inc.