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Article type: Review Article
Authors: Proserpio, Paolaa | Arnaldi, Dariob; c | Nobili, Flaviob; c | Nobili, Linoa; b; *
Affiliations: [a] Centre of Sleep Medicine, Department of Neuroscience, Niguarda Hospital, Milan, Italy | [b] Department of Neuroscience (DINOGMI), University of Genoa, Italy | [c] Clinical of Neurology, Polyclinic San Martino Hospital, Genoa, Italy
Correspondence: [*] Correspondence to: Lino Nobili, Department of Neuroscience, Centre of Sleep Medicine, Niguarda Hospital, Piazza Ospedale Maggiore, 3, 20162, Milan, Italy. Tel.: +39 0264447323; Fax: +39 0264442868; E-mails: lino.nobili@ospedaleniguarda.it and lino.nobili@gmail.com.
Abstract: Sleep represents an active phenomenon regulated by a highly integrated network of cortical and subcortical structures. This complex model results in disruptions at various levels during physiological aging and more deeply during neurodegenerative disorders, thus leading to different sleep alterations. In Alzheimer’s disease (AD), sleep-wake abnormalities were described to occur even in the preclinical phase, thus suggesting they could be a possible AD biomarker. On the other hand, they also favor the progression of the disease. In this paper, we review current theories regarding sleep regulations and functions to highlight the pathophysiological mechanisms at the basis of the bidirectional relationship between sleep and AD. A better understanding of these complex interactions might also be useful to target both sleep disorder management and AD-related symptoms.
Keywords: Aging, circadian process, homeostatic process, melatonin, sleep
DOI: 10.3233/JAD-180041
Journal: Journal of Alzheimer's Disease, vol. 63, no. 3, pp. 871-886, 2018
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