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Genetic overlap between bipolar illness and event-related potentials

Published online by Cambridge University Press:  16 January 2007

MEI-HUA HALL ,
FRÜHLING RIJSDIJK ,
SRIDEVI KALIDINDI ,
KATJA SCHULZE ,
EUGENIA KRAVARITI ,
FERGUS KANE ,
PAK SHAM ,
ELVIRA BRAMON  and
ROBIN M. MURRAY
MEI-HUA HALL
Affiliation:
Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, UK Harvard Medical School, Psychology Research Laboratory, McLean Hospital, Belmont, MA, USA
FRÜHLING RIJSDIJK
Affiliation:
Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, UK
SRIDEVI KALIDINDI
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
KATJA SCHULZE
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
EUGENIA KRAVARITI
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
FERGUS KANE
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
PAK SHAM
Affiliation:
Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, UK Department of Psychiatry, University of Hong Kong, Hong Kong, SAR
ELVIRA BRAMON
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
ROBIN M. MURRAY
Affiliation:
Division of Psychological Medicine, Institute of Psychiatry, King's College London, UK
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Abstract

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Background. Electrophysiological endophenotypes are far less explored in bipolar disorder as compared to schizophrenia. No previous twin study of event-related potentials (ERPs) in bipolar illness has been reported. This study uses a twin design and advanced genetic model fitting analyses aiming to (1) assess and quantify the relationship of a range of ERP components with bipolar disorder with psychotic features, and (2) examine the source of the relationship (due to genetic or environmental factors).

Method. P300, P50 suppression and mismatch negativity (MMN) were recorded in 10 discordant monozygotic (MZ) bipolar twin pairs, six concordant MZ bipolar twin pairs and 78 control twin pairs. Statistical analyses were based on structural equation modelling.

Results. Bipolar disorder was significantly associated with smaller P300 amplitude and decreased P50 suppression. Genetic correlations were the main source of the associations, estimated to be −0·33 for P300 amplitude and 0·46 for P50 ratio. Individual-specific environmental influences were not significant. MMN and P300 latency were not associated with the illness.

Conclusions. The results provide supporting evidence that P300 amplitude and P50 suppression ratio are ERP endophenotypes for bipolar disorder.

Type
Original Article
Information
Psychological Medicine , Volume 37 , Issue 5 , May 2007 , pp. 667 - 678
Copyright
2007 Cambridge University Press