Longitudinal alterations of executive function in non-psychotic adolescents at familial risk for schizophrenia

Tejas S. Bhojraj, Vaibhav A. Diwadkar, John A. Sweeney, Konasale M. Prasad, Shaun M. Eack, Debra M. Montrose, Matcheri S. Keshavan

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Genetic diathesis to schizophrenia may involve alterations of adolescent neurodevelopment manifesting as cognitive deficits. Brain regions mediating executive function (fronto-striatal circuits) develop during adolescence while those supporting elementary aspects of attention (e.g. sustained focused attention) have a more protracted maturation beginning in childhood. We hence predicted that adolescents at risk for schizophrenia would show a failure of normal maturation of executive function. We prospectively assessed 18 offspring and 6 siblings of schizophrenia patients (HR) and 28 healthy controls at baseline, year-1 and year-2 follow-up using the Continuous Performance Test [visual-d'] and Wisconsin Card Sort Test (WCST). Perseverative errors on the WCST in HR remained stable but decreased in controls over the follow-up (study-group by assessment-time interaction, p=0.01, controlling for IQ). No significant study-group by assessment-time interactions were seen for sustained attentional performance. HR may not improve while healthy subjects progressively improve on executive function during adolescence and early adulthood. Our results suggest an altered maturational trajectory of executive function during adolescence in individuals at familial risk for schizophrenia.

Original languageEnglish (US)
Pages (from-to)469-474
Number of pages6
JournalProgress in Neuro-Psychopharmacology and Biological Psychiatry
Volume34
Issue number3
DOIs
StatePublished - Apr 2010

Keywords

  • Attention
  • Executive function
  • Relatives
  • Schizophrenia

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry

Fingerprint Dive into the research topics of 'Longitudinal alterations of executive function in non-psychotic adolescents at familial risk for schizophrenia'. Together they form a unique fingerprint.

Cite this