Lack of association between COMT gene and deficit/nondeficit schizophrenia

Ikwunga Wonodi, Braxton D. Mitchell, O. Colin Stine, L. Elliot Hong, Amie Elliott, Brian Kirkpatrick, William T. Carpenter, Gunvant K. Thaker, Robert W. Buchanan

Research output: Contribution to journalArticle

Abstract

Background: The dopamine dysregulation hypothesis of schizophrenia posits that positive, negative and cognitive symptoms correlate with cortical/subcortical imbalances in dopaminergic transmission. A functional polymorphism (Val158Met) in the catechol-O-methyltransferase (COMT) gene is implicated in the pathophysiology of schizophrenia by its effect on prefrontal dopamine transmission, and its unique impact on prefrontal cognitive and behavioral phenotypes. Cognitive impairments and negative symptoms in schizophrenia have been hypothesized to be associated with hypodopaminergic states. Schizophrenia patients with the deficit syndrome are characterized by primary enduring negative symptoms, impairment on neurocognitive tasks sensitive to frontal and parietal cortical functioning, and poorer functional outcome compared to non-deficit patients. Methods: Eighty-six schizophrenia cases that met DSM-IV criteria for schizophrenia were recruited. Additional categorization into deficit and nondeficit syndrome was performed using the Schedule for the Deficit Syndrome (SDS). A healthy comparison group (n = 50) matched to cases on age and ethnicity was recruited. Allele and genotype frequencies of the Val158Met polymorphism were compared among healthy controls, and schizophrenia cases with the deficit (n = 21), and nondeficit syndrome (n = 65). Results: There was a significant difference in Val/Val genotype frequencies between schizophrenia cases (combined deficit/nondeficit) and healthy controls (p = 0.004). No significant differences in allele or genotype frequencies were observed between deficit and nondeficit cases. Conclusion: Results from this preliminary analysis failed to show an effect of COMT gene on deficit schizophrenia.

Original languageEnglish (US)
Article number1477
Pages (from-to)1-10
Number of pages10
JournalBehavioral and Brain Functions
Volume2
DOIs
StatePublished - Dec 15 2006
Externally publishedYes

Fingerprint

Catechol O-Methyltransferase
Schizophrenia
Genes
Genotype
Dopamine
Neurobehavioral Manifestations
Gene Frequency
Diagnostic and Statistical Manual of Mental Disorders
Appointments and Schedules
Alleles
Phenotype

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Biological Psychiatry
  • Cognitive Neuroscience

Cite this

Wonodi, I., Mitchell, B. D., Stine, O. C., Hong, L. E., Elliott, A., Kirkpatrick, B., ... Buchanan, R. W. (2006). Lack of association between COMT gene and deficit/nondeficit schizophrenia. Behavioral and Brain Functions, 2, 1-10. [1477]. https://doi.org/10.1186/1744-9081-2-1

Lack of association between COMT gene and deficit/nondeficit schizophrenia. / Wonodi, Ikwunga; Mitchell, Braxton D.; Stine, O. Colin; Hong, L. Elliot; Elliott, Amie; Kirkpatrick, Brian; Carpenter, William T.; Thaker, Gunvant K.; Buchanan, Robert W.

In: Behavioral and Brain Functions, Vol. 2, 1477, 15.12.2006, p. 1-10.

Research output: Contribution to journalArticle

Wonodi, I, Mitchell, BD, Stine, OC, Hong, LE, Elliott, A, Kirkpatrick, B, Carpenter, WT, Thaker, GK & Buchanan, RW 2006, 'Lack of association between COMT gene and deficit/nondeficit schizophrenia', Behavioral and Brain Functions, vol. 2, 1477, pp. 1-10. https://doi.org/10.1186/1744-9081-2-1
Wonodi I, Mitchell BD, Stine OC, Hong LE, Elliott A, Kirkpatrick B et al. Lack of association between COMT gene and deficit/nondeficit schizophrenia. Behavioral and Brain Functions. 2006 Dec 15;2:1-10. 1477. https://doi.org/10.1186/1744-9081-2-1
Wonodi, Ikwunga ; Mitchell, Braxton D. ; Stine, O. Colin ; Hong, L. Elliot ; Elliott, Amie ; Kirkpatrick, Brian ; Carpenter, William T. ; Thaker, Gunvant K. ; Buchanan, Robert W. / Lack of association between COMT gene and deficit/nondeficit schizophrenia. In: Behavioral and Brain Functions. 2006 ; Vol. 2. pp. 1-10.
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