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Triplet repeats and bipolar disorder.
Ian Jones1, Katherine Gordon-Smith, Nick Craddock
1Division of Neuroscience, University of Birmingham, Queen Elizabeth Psychiatric Hospital, Birmingham B15 2QZ, United Kingdom. I.R.Jones@bham.ac.uk
Current Psychiatry Reports
|March 27, 2002
Summary
Anticipation, a disease worsening across generations, is being investigated in bipolar disorder. While some studies suggest a link with unstable DNA repeats, definitive proof is still lacking.
Area of Science:
- Genetics
- Neuroscience
- Psychiatry
Background:
- Anticipation, a phenomenon of earlier disease onset or increased severity across generations, was historically noted in psychiatric illnesses but largely dismissed.
- Renewed interest emerged with the discovery of unstable triplet repeat mutations causing neurodegenerative disorders exhibiting anticipation.
Purpose of the Study:
- To investigate the phenomenon of anticipation in bipolar disorder.
- To explore the potential role of unstable DNA triplet repeats in the genetic etiology of bipolar disorder.
Main Methods:
- Review of recent studies on anticipation in bipolar disorder.
- Analysis of case-control studies using the repeat expansion detection (RED) technique.
- Examination of research on candidate genes containing triplet repeats.
Main Results:
- Conflicting evidence exists regarding anticipation in bipolar disorder, with methodological challenges complicating interpretation.
- Some studies using the repeat expansion detection (RED) technique reported longer repeats in bipolar disorder patients, while others found no association.
- No pathogenic triplet repeat mutation has been definitively identified in the etiology of bipolar disorder despite extensive research.
Conclusions:
- The role of anticipation and triplet repeats in bipolar disorder remains controversial.
- Further research is required to definitively establish or refute the presence of triplet repeat mutations in bipolar disorder.
- Resolution of this controversy hinges on the conclusive demonstration of such mutations in the disease's cause.