Anne B Arnett1, Brianna E Cairney1, Arianne S Wallace1, Jennifer Gerdts1, Tychele N Turner2, Evan E Eichler3, Raphael A Bernier1,4. 1. Department of Psychiatry, University of Washington, Seattle, WA, USA. 2. Department of Genome Sciences, University of Washington, Seattle, WA, USA. 3. Department of Genome Sciences, Howard Hughes Medical Institute, University of Washington, Seattle, WA, USA. 4. Center on Human Development and Disability, University of Washington, Seattle, WA, USA.
Abstract
BACKGROUND: Symptoms of autism spectrum disorder (ASD) and inattention (IA) are highly comorbid and associated with deficits in executive cognition. Cognitive deficits have been posited as candidate endophenotypes of psychiatric traits, but few studies have conceptualized cognitive deficits as psychiatric comorbidities. The latter model is consistent with a latent factor reflecting broader liability to neuropsychological dysfunction, and explains heterogeneity in the cognitive profile of individuals with ASD and IA. METHODS: We tested competing models of covariance among symptoms of ASD, IA, and cognition in a sample of 73 youth with a known genetic mutation. RESULTS: A common executive factor fit best as a cognitive comorbidity, rather than endophenotype, of the shared variance between measures of IA and ASD symptoms. Known genetic risk explained a third of the shared variance among psychiatric and cognitive measures. CONCLUSIONS: Comorbid symptoms of ASD, IA, and cognitive deficits are likely influenced by common neurogenetic factors. Known genetic risk in ASD may inform future investigation of putative genetic causes of IA.
BACKGROUND: Symptoms of autism spectrum disorder (ASD) and inattention (IA) are highly comorbid and associated with deficits in executive cognition. Cognitive deficits have been posited as candidate endophenotypes of psychiatric traits, but few studies have conceptualized cognitive deficits as psychiatric comorbidities. The latter model is consistent with a latent factor reflecting broader liability to neuropsychological dysfunction, and explains heterogeneity in the cognitive profile of individuals with ASD and IA. METHODS: We tested competing models of covariance among symptoms of ASD, IA, and cognition in a sample of 73 youth with a known genetic mutation. RESULTS: A common executive factor fit best as a cognitive comorbidity, rather than endophenotype, of the shared variance between measures of IA and ASD symptoms. Known genetic risk explained a third of the shared variance among psychiatric and cognitive measures. CONCLUSIONS: Comorbid symptoms of ASD, IA, and cognitive deficits are likely influenced by common neurogenetic factors. Known genetic risk in ASD may inform future investigation of putative genetic causes of IA.
Authors: Sandra Weintraub; Sureyya S Dikmen; Robert K Heaton; David S Tulsky; Philip D Zelazo; Patricia J Bauer; Noelle E Carlozzi; Jerry Slotkin; David Blitz; Kathleen Wallner-Allen; Nathan A Fox; Jennifer L Beaumont; Dan Mungas; Cindy J Nowinski; Jennifer Richler; Joanne A Deocampo; Jacob E Anderson; Jennifer J Manly; Beth Borosh; Richard Havlik; Kevin Conway; Emmeline Edwards; Lisa Freund; Jonathan W King; Claudia Moy; Ellen Witt; Richard C Gershon Journal: Neurology Date: 2013-03-12 Impact factor: 9.910
Authors: Brian J O'Roak; Pelagia Deriziotis; Choli Lee; Laura Vives; Jerrod J Schwartz; Santhosh Girirajan; Emre Karakoc; Alexandra P Mackenzie; Sarah B Ng; Carl Baker; Mark J Rieder; Deborah A Nickerson; Raphael Bernier; Simon E Fisher; Jay Shendure; Evan E Eichler Journal: Nat Genet Date: 2011-05-15 Impact factor: 38.330