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Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome.

Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Research Abstract Details 

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  • Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Abstract Text:

    doron gothelfDoron Gothelf,fumiko hoeftFumiko Hoeft,christine hinardChristine Hinard,joachim f hallmayerJoachim F Hallmayer,john van dover stoeckerJohn Van Dover Stoecker,stylianos e antonarakisStylianos E Antonarakis,michael a morrisMichael A Morris,allan l reissAllan L Reiss,

    22q11.2 deletion syndrome (22q11.2DS) is a well-known genetic risk factor for schizophrenia. The catechol-O-methyltransferase (COMT) gene falls within the 22q11.2 minimal critical region of the deletion. Brain activity, as measured by functional magnetic resonance imaging (fMRI) during a Go/NoGo, response inhibition task was assessed in adolescents with 22q11.2DS (n = 13), typically developing (TD) controls (n = 14), and controls with developmental disability (DD, n = 9). Subjects with 22q11.2DS were also genotyped for the COMT Met/Val polymorphism. Groups did not differ on task performance. However, compared to both control groups, the 22q11.2DS group showed greater brain activation within left parietal regions. Comparison of brain activation between 22q11.2DS Met and Val subgroups revealed significantly increased activation (Met>Val) in the cingulate but not the dorsolateral prefrontal cortex. These preliminary findings suggest that adolescents with 22q11.2DS compensate for executive dysfunction via recruitment of parietal regions. Further, the COMT Met subgroup of 22q11.2DS may recruit additional cingulate activation for tasks requiring attention and inhibition. 22q11.2DS is a unique model for learning about the deleterious effects of decreased dosage of the COMT gene on brain function.

    Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Publishing Authors By Initials

    d gothelfD Gothelf,f hoeftF Hoeft,c hinardC Hinard,jf hallmayerJF Hallmayer,jv stoeckerJV Stoecker,se antonarakisSE Antonarakis,ma morrisMA Morris,al reissAL Reiss,

    For similar amino acids, peptides, and proteins: amino acids: amino acids, branched-chain: valine research abstracts see: amino acids, peptides, and proteins: amino acids: amino acids, branched-chain: valine research

    PUBMED ID PMID:

    MEDLINE DATE:

    Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Human brain mapping

    VOLUME: 28

    Page Numbers: 533-42

    Journal Abbreviation:

    ISSN: 1065-9471

    DAY: 3

    MONTH: Jun

    YEAR: 2007

    Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9419065

    Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Keywords Mesh Terms:

    KEYWORDS: Valine

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome. Information

    Substance Name: Catechol O-Methyltransferase

    Registry Number: EC 2.1.1.6

    Grant and Affiliation Information for Abnormal cortical activation during response inhibition in 22q11.2 deletion syndrome.

    AFFILIATION: The Behavioral Neurogenetics Center, Child Psychiatry Department, Schneider Children's Medical Center of Israel, Petah Tiqwa, Israel. gothelf@post.tau.ac.il

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIMH

    GRANT: MH50047

    ACRONYM: MH

    MEDLINETA: Hum Brain Mapp

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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