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  1. David Breen1,
  2. Romina Vuono1,
  3. Upekshani Nawarathna2,
  4. Kate Fisher1,
  5. John Shneerson2,
  6. Akhilesh Reddy3,
  7. Roger Barker1
  1. 1John van Geest Centre for Brain Repair, University of Cambridge, Cambridge
  2. 2Respiratory and Sleep Support Centre, Papworth Hospital, Cambridge
  3. 3Institute of Metabolic Science, University of Cambridge, Cambridge


Aim Sleep disturbances are recognised as a common non-motor complaint in Parkinson's disease but their aetiology is poorly understood. We set out to define the sleep and circadian phenotype of early-stage Parkinson's disease patients.

Methods We began by assessing the sleep characteristics of a large population-representative incident Parkinson's disease cohort (n=239) at the University of Cambridge. We went on to carry out more comprehensive case-control sleep assessments in a subgroup of these patients (n=30) and matched controls (n=15). Outcome measures were sleep diagnoses and sleep architecture based on polysomnography studies; actigraphy assessment; and 24-hour analyses of serum cortisol, melatonin and peripheral clock gene expression (Bmal1, Per2, and Rev-Erbα).

Results Subjective sleep complaints were present in almost half of newly-diagnosed patients and correlated significantly with poorer quality of life. Parkinson's disease patients exhibited increased sleep latency, reduced sleep efficiency and reduced REM sleep. In addition, there was a sustained elevation of serum cortisol levels, reduced circulating melatonin levels, and altered Bmal1 expression in Parkinson's disease patients compared to controls.

Conclusions The sleep dysfunction seen in early Parkinson's disease may reflect a more fundamental pathology in the molecular clock underlying circadian rhythms.

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