Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk

22q11.2 deletion syndrome (also known as DiGeorge syndrome or velo-cardio-facial syndrome) is characterized by increased vulnerability to neuropsychiatric symptoms, with approximately 30% of individuals with the deletion going on to develop schizophrenia. Clinically, deficits in executive function h...

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Main Authors: Ana A. Francisco, Douwe J. Horsthuis, Maryann Popiel, John J. Foxe, Sophie Molholm
Format: Article
Language:English
Published: Elsevier 2020-01-01
Series:NeuroImage: Clinical
Subjects:
EEG
P3
Ne
Pe
Online Access:http://www.sciencedirect.com/science/article/pii/S2213158220301881
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spelling doaj-a67c4496a79c40a1bfeec8b72d18b0c92020-11-25T03:38:39ZengElsevierNeuroImage: Clinical2213-15822020-01-0127102351Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and riskAna A. Francisco0Douwe J. Horsthuis1Maryann Popiel2John J. Foxe3Sophie Molholm4The Cognitive Neurophysiology Laboratory, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Neuroscience, Rose F. Kennedy Center, Albert Einstein College of Medicine, Bronx, NY, USA; Corresponding authors at: Albert Einstein College of Medicine, Van Etten Building, Suite 1C, 1225 Morris Park Avenue, Bronx, NY 1046, USA.The Cognitive Neurophysiology Laboratory, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USADepartment of Psychiatry, Jacobi Medical Center, Bronx, NY, USAThe Cognitive Neurophysiology Laboratory, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Neuroscience, Rose F. Kennedy Center, Albert Einstein College of Medicine, Bronx, NY, USA; The Cognitive Neurophysiology Laboratory, Department of Neuroscience, The Ernest J. Del Monde Institute for Neuroscience, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USAThe Cognitive Neurophysiology Laboratory, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Neuroscience, Rose F. Kennedy Center, Albert Einstein College of Medicine, Bronx, NY, USA; The Cognitive Neurophysiology Laboratory, Department of Neuroscience, The Ernest J. Del Monde Institute for Neuroscience, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA; Corresponding authors at: Albert Einstein College of Medicine, Van Etten Building, Suite 1C, 1225 Morris Park Avenue, Bronx, NY 1046, USA.22q11.2 deletion syndrome (also known as DiGeorge syndrome or velo-cardio-facial syndrome) is characterized by increased vulnerability to neuropsychiatric symptoms, with approximately 30% of individuals with the deletion going on to develop schizophrenia. Clinically, deficits in executive function have been noted in this population, but the underlying neural processes are not well understood. Using a Go/No-Go response inhibition task in conjunction with high-density electrophysiological recordings (EEG), we sought to investigate the behavioral and neural dynamics of inhibition of a prepotent response (a critical component of executive function) in individuals with 22q11.2DS with and without psychotic symptoms, when compared to individuals with idiopathic schizophrenia and age-matched neurotypical controls. Twenty-eight participants diagnosed with 22q11.2DS (14–35 years old; 14 with at least one psychotic symptom), 15 individuals diagnosed with schizophrenia (18–63 years old) and two neurotypical control groups (one age-matched to the 22q11.2DS sample, the other age-matched to the schizophrenia sample) participated in this study. Analyses focused on the N2 and P3 no-go responses and error-related negativity (Ne) and positivity (Pe). Atypical inhibitory processing was shown behaviorally and by significantly reduced P3, Ne, and Pe responses in 22q11.2DS and schizophrenia. Interestingly, whereas P3 was only reduced in the presence of psychotic symptoms, Ne and Pe were equally reduced in schizophrenia and 22q11.2DS, regardless of the presence of symptoms. We argue that while P3 may be a marker of disease severity, Ne and Pe might be candidate markers of risk.http://www.sciencedirect.com/science/article/pii/S2213158220301881Go/No-GoEEGVisual event-related potentialsP3NePe
collection DOAJ
language English
format Article
sources DOAJ
author Ana A. Francisco
Douwe J. Horsthuis
Maryann Popiel
John J. Foxe
Sophie Molholm
spellingShingle Ana A. Francisco
Douwe J. Horsthuis
Maryann Popiel
John J. Foxe
Sophie Molholm
Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
NeuroImage: Clinical
Go/No-Go
EEG
Visual event-related potentials
P3
Ne
Pe
author_facet Ana A. Francisco
Douwe J. Horsthuis
Maryann Popiel
John J. Foxe
Sophie Molholm
author_sort Ana A. Francisco
title Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
title_short Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
title_full Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
title_fullStr Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
title_full_unstemmed Atypical response inhibition and error processing in 22q11.2 Deletion Syndrome and schizophrenia: Towards neuromarkers of disease progression and risk
title_sort atypical response inhibition and error processing in 22q11.2 deletion syndrome and schizophrenia: towards neuromarkers of disease progression and risk
publisher Elsevier
series NeuroImage: Clinical
issn 2213-1582
publishDate 2020-01-01
description 22q11.2 deletion syndrome (also known as DiGeorge syndrome or velo-cardio-facial syndrome) is characterized by increased vulnerability to neuropsychiatric symptoms, with approximately 30% of individuals with the deletion going on to develop schizophrenia. Clinically, deficits in executive function have been noted in this population, but the underlying neural processes are not well understood. Using a Go/No-Go response inhibition task in conjunction with high-density electrophysiological recordings (EEG), we sought to investigate the behavioral and neural dynamics of inhibition of a prepotent response (a critical component of executive function) in individuals with 22q11.2DS with and without psychotic symptoms, when compared to individuals with idiopathic schizophrenia and age-matched neurotypical controls. Twenty-eight participants diagnosed with 22q11.2DS (14–35 years old; 14 with at least one psychotic symptom), 15 individuals diagnosed with schizophrenia (18–63 years old) and two neurotypical control groups (one age-matched to the 22q11.2DS sample, the other age-matched to the schizophrenia sample) participated in this study. Analyses focused on the N2 and P3 no-go responses and error-related negativity (Ne) and positivity (Pe). Atypical inhibitory processing was shown behaviorally and by significantly reduced P3, Ne, and Pe responses in 22q11.2DS and schizophrenia. Interestingly, whereas P3 was only reduced in the presence of psychotic symptoms, Ne and Pe were equally reduced in schizophrenia and 22q11.2DS, regardless of the presence of symptoms. We argue that while P3 may be a marker of disease severity, Ne and Pe might be candidate markers of risk.
topic Go/No-Go
EEG
Visual event-related potentials
P3
Ne
Pe
url http://www.sciencedirect.com/science/article/pii/S2213158220301881
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