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Journal of Aging Research
Volume 2011, Article ID 383091, 4 pages
Review Article

CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease

1Department of Psychiatry, University of Rostock, Gehlsheimerstraße 20, 18147 Rostock, Germany
2Department of Psychology, National University of Ireland, Maynooth, Maynooth, Ireland
3Biochemistry and Proteomics Group, Department of Chemistry and Biomolecular Science, Clarkson University, Potsdam, NY 13699, USA
4Department of Child and Adolescent Psychiatry and Neurology, University of Rostock, 18147 Rostock, Germany

Received 2 August 2011; Accepted 16 August 2011

Academic Editor: Aurel Popa-Wagner

Copyright © 2011 J. Thome et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Disturbed circadian rhythms with sleep problems and disrupted diurnal activity are often seen in patients suffering from Alzheimer disease (AD). Both endogenous CLOCK genes and external Zeitgeber are responsible for the maintenance of circadian rhythmicity in humans. Therefore, modifications of the internal CLOCK system and its interactions with exogenous factors might constitute the neurobiological basis for clinically observed disruptions in rhythmicity, which often have grave consequences for the quality of life of patients and their caregivers. Presently, more and more data are emerging demonstrating how alterations of the CLOCK gene system might contribute to the pathophysiology of AD and other forms of dementia. At the same time, the impact of neuropsychiatric medication on CLOCK gene expression is under investigation.