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Investigation of circadian disruption in bipolar disorder

Published online by Cambridge University Press:  24 June 2014

J Fullerton,
A Heath,
P Mitchell and
P Schofield
J Fullerton
Affiliation:
Prince of Wales Medical Research Institute
A Heath
Affiliation:
Prince of Wales Medical Research Institute
P Mitchell
Affiliation:
Mood Disorders Unit, The Black Dog Institute, Sydney, Australia
P Schofield
Affiliation:
Prince of Wales Medical Research Institute
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Abstract

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Information

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006, pp. 251
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

There is a growing body of evidence implicating circadian disruption as a possible mechanism underlying the pathogenesis of bipolar disorder. The circadian clock is entrained by changes in our external environment and regulates many of our bodies functions, including our sleep-wake cycle, metabolism, thermoregulation and blood pressure. While the measurement of circadian rhythmicity in mice is relatively straight forward through automated recording of home cage activity, the measurement of circadian function/disruption in humans is more difficult and costly, requiring each patient to undergo actigraphy in a sleep laboratory over a period of several days.

Methods:

To collect data on a scale sufficient for genetic studies, a more efficient method of monitoring circadian function in humans is required to determine whether circadian disruption is involved in the primary pathogenesis of bipolar disorder or whether symptomatic sleep disruption is a secondary defect. We are investigating the role of circadian disruption in bipolar disorder, by genetic association, and rhythmic gene expression using immortalized B lymphocytes from a cohort of Australian bipolar families.

Results:

Circadian timing in immortalized B lymphocytes is synchronized by serum shock, and circa-dian gene expression ensues for at least 56 h post synchronization.

Conclusions:

Peripheral tissues, including immortalized blood cells, can be used as a cheap and higher throughput method to measure circadian output in humans and will be a useful adjunct to elucidating the molecular mechanisms underlying bipolar disorder.