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Sleep and EEG as biological markers in animal models of Huntington's disease

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Summary: Although abnormal circadian rhythmicity has been demonstrated in both human patients and in rodent models of Huntington’s disease (HD), a comprehensive description of sleep and electroencephalogram (EEG) changes has never been conducted.

Here we studied sleep and EEG disturbances in a transgenic mouse model of HD (R6/2 mice). We implanted EEG and electromyogram electrodes into male and female R6/2 mice and their wild-type (WT) littermates and then recorded baseline sleep/wake behaviour at pre-symptomatic, symptomatic, and late stages of the disease. In addition, we treated a subgroup of late stage HD mice with the tricyclic antidepressant amitriptyline or vehicle at dark onset, and recorded subsequent sleep/wake behaviour.

We found that sleep and EEG were already significantly disrupted in R6/2 mice at the pre-symptomatic stage. The disturbances worsened with age, so that symptomatic, R6/2 mice were unable to maintain long periods of wakefulness and had an increased propensity for rapid eye movement (REM) sleep. As the disease progressed, an abnormal EEG gamma activity emerged in R6/2 mice, irrespective of sleep states. Treatment with amitriptyline increased non-REM sleep amount, reduced wake and REM sleep amount in both WT and R6/2 mice, and attenuated EEG gamma activity in R6/2 mice.

Our results suggest that a decreased monoaminergic activity may be responsible for some of the sleep and EEG symptoms found in R6/2 mice. If similar changes occur in humans, these early and progressive sleep and EEG abnormalities could serve as biological markers of HD.

Biographical note: Sandor joined the laboratory of Professor Jenny Morton in the spring of 2011. His main interest currently is in sleep and EEG patterns in Huntington’s disease (HD), and how abnormalities in these patterns might be corrected pharmacologically. He has previously worked at the Institute of Experimental Medicine of The Hungarian Academy of Sciences, the Beth Israel Deaconess Medical Center and the National Institute of Psychiatry and Neurology in Budapest.

This talk is part of the Madingley Lunchtime Seminars series.

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