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Dissociable genetic contributions to error processing: a multimodal neuroimaging study.

Yigal Agam1, Mark Vangel2, Joshua L Roffman3

  • 1Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Athinoula A. Martinos Center for Biomedical Imaging, Harvard Medical School, Charlestown, Massachusetts, United States of America.

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Summary

The dopamine D4 receptor (DRD4) gene variant, but not the MTHFR gene variant, significantly influenced the error-related negativity (ERN) and dorsal anterior cingulate cortex (dACC) activation differently, suggesting distinct neural and genetic underpinnings for these error markers.

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Area of Science:

  • Neuroscience
  • Genetics
  • Cognitive Psychology

Background:

  • Neuroimaging identifies two error commission markers: error-related negativity (ERN) and dorsal anterior cingulate cortex (dACC) activation.
  • Recent evidence suggests ERN originates from the posterior cingulate cortex, distinct from dACC.
  • This study investigates if these error markers have different genetic mediation.

Purpose of the Study:

  • To test the hypothesis that ERN and dACC activation have different genetic mediation.
  • To examine the differential effects of specific gene polymorphisms on these two error markers.

Main Methods:

  • Measured ERN and dACC activation in 92 participants (healthy and clinical diagnoses).
  • Utilized functional MRI, magnetoencephalography, and electroencephalography during an error-commission task.
  • Analyzed mediation by dopamine D4 receptor (DRD4) C-521T and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms.

Main Results:

  • Replicated posterior cingulate source for ERN across healthy, schizophrenia, and OCD groups.
  • DRD4 C-521T allele load significantly affected ERN amplitude but not dACC activation.
  • MTHFR C677T allele load significantly affected dACC activation but not ERN amplitude.

Conclusions:

  • DRD4 C-521T demonstrated a significant differential effect on ERN and dACC activation.
  • Findings support distinct neural and genetic mediation for ERN and dACC error markers.
  • Suggests that ERN and dACC activation represent separate processes in error commission.