N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth

Highly penetrant mutations leading to schizophrenia are enriched for genes coding for N-methyl-D-aspartate receptor signaling complex (NMDAR-SC), implicating plasticity defects in the disease’s pathogenesis. The importance of plasticity in neurodevelopment implies a role for therapies that target th...

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Main Authors: Joseph Gonzalez-Heydrich, Michelle Bosquet Enlow, Eugene D’Angelo, Larry J. Seidman, Sarah Gumlak, April Kim, Kristen A. Woodberry, Ashley Rober, Sahil Tembulkar, Kyle O’Donnell, Hesham M. Hamoda, Kara Kimball, Alexander Rotenberg, Lindsay M. Oberman, Alvaro Pascual-Leone, Matcheri S. Keshavan, Frank H. Duffy
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2016/4209831
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author Joseph Gonzalez-Heydrich
Michelle Bosquet Enlow
Eugene D’Angelo
Larry J. Seidman
Sarah Gumlak
April Kim
Kristen A. Woodberry
Ashley Rober
Sahil Tembulkar
Kyle O’Donnell
Hesham M. Hamoda
Kara Kimball
Alexander Rotenberg
Lindsay M. Oberman
Alvaro Pascual-Leone
Matcheri S. Keshavan
Frank H. Duffy
author_facet Joseph Gonzalez-Heydrich
Michelle Bosquet Enlow
Eugene D’Angelo
Larry J. Seidman
Sarah Gumlak
April Kim
Kristen A. Woodberry
Ashley Rober
Sahil Tembulkar
Kyle O’Donnell
Hesham M. Hamoda
Kara Kimball
Alexander Rotenberg
Lindsay M. Oberman
Alvaro Pascual-Leone
Matcheri S. Keshavan
Frank H. Duffy
author_sort Joseph Gonzalez-Heydrich
collection DOAJ
description Highly penetrant mutations leading to schizophrenia are enriched for genes coding for N-methyl-D-aspartate receptor signaling complex (NMDAR-SC), implicating plasticity defects in the disease’s pathogenesis. The importance of plasticity in neurodevelopment implies a role for therapies that target these mechanisms in early life to prevent schizophrenia. Testing such therapies requires noninvasive methods that can assess engagement of target mechanisms. The auditory N100 is an obligatory cortical response whose amplitude decreases with tone repetition. This adaptation may index the health of plasticity mechanisms required for normal development. We exposed participants aged 5 to 17 years with psychosis n=22, at clinical high risk (CHR) for psychosis n=29, and healthy controls n=17 to an auditory tone repeated 450 times and measured N100 adaptation (mean amplitude during first 150 tones − mean amplitude during last 150 tones). N100 adaptation was reduced in CHR and psychosis, particularly among participants <13 years old. Initial N100 blunting partially accounted for differences. Decreased change in the N100 amplitude with tone repetition may be a useful marker of defects in neuroplastic mechanisms measurable early in life.
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spelling doaj-art-38ac93c4efaa43dba90e8e03e44ec71e2025-02-03T07:25:36ZengWileyNeural Plasticity2090-59041687-54432016-01-01201610.1155/2016/42098314209831N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic YouthJoseph Gonzalez-Heydrich0Michelle Bosquet Enlow1Eugene D’Angelo2Larry J. Seidman3Sarah Gumlak4April Kim5Kristen A. Woodberry6Ashley Rober7Sahil Tembulkar8Kyle O’Donnell9Hesham M. Hamoda10Kara Kimball11Alexander Rotenberg12Lindsay M. Oberman13Alvaro Pascual-Leone14Matcheri S. Keshavan15Frank H. Duffy16Boston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USADepartment of Psychiatry, Harvard Medical School, 401 Park Drive, Boston, MA 02215, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USADepartment of Psychiatry, Harvard Medical School, 401 Park Drive, Boston, MA 02215, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USANeuroplasticity and Autism Spectrum Disorder Program and Department of Psychiatry and Human Behavior, E.P. Bradley Hospital and Warren Alpert Medical School, Brown University, 1011 Veterans Memorial Parkway, East Providence, RI 02915, USADepartment of Psychiatry, Commonwealth Research Center, Beth Israel Deaconess Medical Center, 75 Fenwood Road, Boston, MA 02115, USADepartment of Psychiatry, Harvard Medical School, 401 Park Drive, Boston, MA 02215, USABoston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USAHighly penetrant mutations leading to schizophrenia are enriched for genes coding for N-methyl-D-aspartate receptor signaling complex (NMDAR-SC), implicating plasticity defects in the disease’s pathogenesis. The importance of plasticity in neurodevelopment implies a role for therapies that target these mechanisms in early life to prevent schizophrenia. Testing such therapies requires noninvasive methods that can assess engagement of target mechanisms. The auditory N100 is an obligatory cortical response whose amplitude decreases with tone repetition. This adaptation may index the health of plasticity mechanisms required for normal development. We exposed participants aged 5 to 17 years with psychosis n=22, at clinical high risk (CHR) for psychosis n=29, and healthy controls n=17 to an auditory tone repeated 450 times and measured N100 adaptation (mean amplitude during first 150 tones − mean amplitude during last 150 tones). N100 adaptation was reduced in CHR and psychosis, particularly among participants <13 years old. Initial N100 blunting partially accounted for differences. Decreased change in the N100 amplitude with tone repetition may be a useful marker of defects in neuroplastic mechanisms measurable early in life.http://dx.doi.org/10.1155/2016/4209831
spellingShingle Joseph Gonzalez-Heydrich
Michelle Bosquet Enlow
Eugene D’Angelo
Larry J. Seidman
Sarah Gumlak
April Kim
Kristen A. Woodberry
Ashley Rober
Sahil Tembulkar
Kyle O’Donnell
Hesham M. Hamoda
Kara Kimball
Alexander Rotenberg
Lindsay M. Oberman
Alvaro Pascual-Leone
Matcheri S. Keshavan
Frank H. Duffy
N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
Neural Plasticity
title N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
title_full N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
title_fullStr N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
title_full_unstemmed N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
title_short N100 Repetition Suppression Indexes Neuroplastic Defects in Clinical High Risk and Psychotic Youth
title_sort n100 repetition suppression indexes neuroplastic defects in clinical high risk and psychotic youth
url http://dx.doi.org/10.1155/2016/4209831
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