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Single nucleotide polymorphism heritability and differential patterns of genetic overlap between inattention and four neurocognitive factors in youth

Published online by Cambridge University Press:  21 January 2020

Lauren Micalizzi Open the ORCID record for Lauren Micalizzi [Opens in a new window] ,
Leslie A. Brick ,
Marisa E. Marraccini ,
Chelsie E. Benca-Bachman ,
Rohan H.C. Palmer  and
Valerie S. Knopik
Lauren Micalizzi*
Affiliation:
Center for Alcohol and Addiction Studies, Brown University, Providence, RI, USA Department of Psychology, University of Saint Joseph, West Hartford, CT, USA
Leslie A. Brick
Affiliation:
Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Providence, RI, USA
Marisa E. Marraccini
Affiliation:
School of Education, University of North Carolina Chapel Hill, Chapel Hill, NC, USA
Chelsie E. Benca-Bachman
Affiliation:
Department of Psychology, Emory University, Atlanta, GA, USA
Rohan H.C. Palmer
Affiliation:
Department of Psychology, Emory University, Atlanta, GA, USA
Valerie S. Knopik
Affiliation:
Department of Human Development and Family Studies, Purdue University, West Lafayette, IN, USA
*
Author for Correspondence: Lauren Micalizzi, Ph.D. University of Saint Joseph, Department of Psychology, 1678 Asylum Avenue, West Hartford, CT, 06117; E-mail: lmicalizzi@usj.edu.
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Abstract

Theoretical models of attention-deficit/hyperactivity disorder implicate neurocognitive dysfunction, yet neurocognitive functioning covers a range of abilities that may not all be linked with inattention. This study (a) investigated the single nucleotide polymorphism (SNP) heritability (h2SNP) of inattention and aspects of neurocognitive efficiency (memory, social cognition, executive function, and complex cognition) based on additive genome-wide effects; (b) examined if there were shared genetic effects among inattention and each aspect of neurocognitive efficiency; and (c) conducted an exploratory genome-wide association study to identify genetic regions associated with inattention. The sample included 3,563 participants of the Philadelphia Neurodevelopmental Cohort, a general population sample aged 8–21 years who completed the Penn Neurocognitive Battery. Data on inattention was obtained with the Kiddie Schedule of Affective Disorders (adapted). Genomic relatedness matrix restricted maximum likelihood was implemented in genome-wide complex trait analysis. Analyses revealed significant h2SNP for inattention (20%, SE = 0.08), social cognition (13%, SE = 0.08), memory (17%, SE = 0.08), executive function (25%, SE = 0.08), and complex cognition (24%, SE = 0.08). There was a positive genetic correlation (0.67, SE = 0.37) and a negative residual covariance (−0.23, SE = 0.06) between inattention and social cognition. No SNPs reached genome-wide significance for inattention. Results suggest specificity in genetic overlap among inattention and different aspects of neurocognitive efficiency.

Keywords

adolescenceGCTAgeneticsheritabilityinattentionneurocognitive functioning
Type
Regular Articles
Information
Development and Psychopathology , Volume 33 , Issue 1 , February 2021 , pp. 76 - 86
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Copyright © Cambridge University Press 2020

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