Emma J. Wams, Gordon K. Wilcock, Russell G. Foster and Katharina Wulff* Pages 1030 - 1041 ( 12 )
Objective: Age-related cognitive impairment and the prevalence of neurodegenerative disease contribute to decreasing quality of life in affected individuals and their families as well as demand considerable societal responsibility. Sleep supports overall brain activity and contributes to both physical and mental health. As a result, sleep is an attractive target for exploring ways to promote health in accelerated cognitive aging. The aims of this study were to characterise cognitive performance and sleepwake behaviour in older adults with different degrees of cognitive impairment.Methods: Cognitive ability in a variety of domains of amnestic mild cognitive impairment (aMCI) individuals, moderate AD patients and cognitively healthy adults was assessed with the Mini-Mental-State- Examination and five computerised tests (CANTABeclipse™). It was imperative to exclude mixed diagnosis, comorbidities (psychiatric, neurological, sleep disorders), anti-dementia medication, institutionalised subjects, and to study participants within their home to minimise confounders. Sleep profiles were assessed with the Jupiter Sleep Questionnaire and Pittsburgh Sleep Quality Index completed by participants and carers. Participants’ sleep-wake activity was monitored for three weeks using a wrist-worn actigraph and a semi-standardised diary. Groups were compared according to their diagnostic category and then pooled to correlate sleep data with cognitive performance. Results: Mild cognitive impairment in aMCI individuals was reflected in domains of verbal and visuospatial memory but not attentional capacity or episodic memory. All self-reported and objective measures of sleep quality and sleep quantity of the aMCIs were within the normal range and comparable to those of cognitively healthy controls. Moderate AD patients scored significantly lower on all cognitive tests and had lower rest-activity amplitudes and distinctively longer nightly sleep periods that were not associated with sleep disorders, sleep medication or poor sleep efficiency. Self-rated and actigraphic quality of sleep was equally good (i.e. 90% sleep efficiency) in all groups. Conclusion: This investigation is of clinical importance, because major confounding variables were excluded. The lack of comorbidities might be responsible for the absence of sundown syndrome and sleep disturbances commonly reported in AD patients. Whether there is interdependence between progressive decline in cognition and long sleep duration remains elusive. Future studies should address whether prolonged sleep at night and decreased day-time activity can be altered to delay the progression of cognitive decline.
Sleep, rest-activity rhythms, aging, amnestic, dementia, cognition, CANTAB, actigraphy.
Nuffield Department of Clinical Neurosciences, Oxford Molecular Pathology Institute (OMPI), South Parks Road, Oxford, OX1 3RE, Nuffield Department of Clinical Neurosciences, West Wing, University of Oxford, John Radcliffe Hospital, Headington, Oxford OX3 9DU, Nuffield Department of Clinical Neurosciences, Oxford Molecular Pathology Institute (OMPI), South Parks Road, Oxford, OX1 3RE, University of Oxford, Sleep and Circadian Neuroscience Institute, Sir William Dunn School of Pathology (OMPI), South Parks Road, Oxford OX1 3RE