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DISC1 Ser704Cys impacts thalamic-prefrontal connectivity.

Bing Liu1, Lingzhong Fan, Yue Cui

  • 1Brainnetome Center, Institute of Automation, Chinese Academy of Sciences, Beijing, 100190, China.

Brain Structure & Function
|October 23, 2013
PubMed
Summary

The DISC1 Ser704Cys gene variant impacts brain connectivity, specifically altering thalamic-prefrontal circuits. This finding offers insights into the neural basis of psychiatric disorders linked to DISC1.

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Area of Science:

  • Neuroscience
  • Genetics
  • Psychiatry

Background:

  • The Disrupted-in-Schizophrenia 1 (DISC1) gene is implicated in psychiatric disorders.
  • The DISC1 Ser704Cys polymorphism is linked to brain structure and function variations.
  • Previous research suggests DISC1 influences brain network efficiency.

Purpose of the Study:

  • To investigate the association between DISC1 Ser704Cys and functional brain connectivity, particularly in thalamic-prefrontal circuits.
  • To explore how this genetic variant affects functional connectivity density (FCD) hubs.

Main Methods:

  • Functional connectivity density (FCD) mapping using functional magnetic resonance imaging (fMRI) data.
  • Analysis of a large cohort of healthy Han Chinese subjects.
  • Examination of both functional and anatomical connectivity between the thalamus and prefrontal cortex.

Main Results:

  • DISC1 Cys-allele carriers exhibited increased long-range functional connectivity hubs in the bilateral thalami compared to Ser homozygotes.
  • Thalamic-prefrontal functional connectivity was significantly increased in Cys-allele carriers.
  • Thalamic-prefrontal anatomical connectivity was decreased in DISC1 Cys-allele carriers.

Conclusions:

  • The DISC1 Ser704Cys polymorphism significantly influences human thalamic-prefrontal circuits.
  • These findings provide a deeper understanding of the neural mechanisms connecting DISC1 to psychiatric disorder risk.
  • The study highlights the role of specific genetic variations in shaping brain network architecture and function.