Linkage of mood disorders with D2, D3 and TH genes: a multicenter study

J Affect Disord. 2000 Apr;58(1):51-61. doi: 10.1016/s0165-0327(99)00112-3.

Abstract

Background: It has been suggested that the dopaminergic system is involved in the pathophysiology of mood disorders. We conducted a multicenter study of families with mood disorders, to investigate a possible linkage with genes coding for dopamine receptor D2, dopamine receptor D3 and tyrosine hydroxylase (TH).

Methods: Twenty three mood disorder pedigrees collected within the framework of the European Collaborative Project on Affective Disorders were analyzed with parametric and non-parametric linkage methods. Various potential phenotypes were considered, from a narrow (only bipolar as affected) to a broad (bipolar+major depressive+schizoaffective disorders) definition of affection status.

Results: Parametric analyses excluded linkage for all the candidate genes, even though small positive LOD (Limit of Detection) scores were observed for TH in three families. Non-parametric analyses yielded negative results for all markers.

Conclusion: The D2 and D3 dopamine receptors were, therefore, not a major liability factor for mood disorders in our sample, whereas TH may play a role in a subgroup of patients.

Publication types

  • Multicenter Study

MeSH terms

  • Bipolar Disorder / diagnosis
  • Bipolar Disorder / genetics*
  • Bipolar Disorder / psychology
  • Depressive Disorder, Major / diagnosis
  • Depressive Disorder, Major / genetics*
  • Depressive Disorder, Major / psychology
  • Europe
  • Gene Expression / physiology
  • Genetic Linkage / genetics*
  • Genetic Markers / genetics
  • Humans
  • Phenotype
  • Psychotic Disorders / diagnosis
  • Psychotic Disorders / genetics*
  • Psychotic Disorders / psychology
  • Receptors, Dopamine D2 / genetics*
  • Receptors, Dopamine D3
  • Tyrosine 3-Monooxygenase / genetics*

Substances

  • DRD3 protein, human
  • Genetic Markers
  • Receptors, Dopamine D2
  • Receptors, Dopamine D3
  • Tyrosine 3-Monooxygenase