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. 2018 Nov 23;9:702. doi: 10.3389/fendo.2018.00702

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Copyright © 2018 Xu, Jackson, Khoury, Escobar and Perez-Pinzon.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SIRT1 levels in the suprachiasmatic nucleus (SCN) are disrupted by aging and Alzheimer's disease. The rhythmic expression of SIRT1 in the SCN has been reported to be disrupted in animal models of aging and Alzheimer's disease. This, in turn, disrupts the circadian expression of clock genes causing a disruption in the activity patterns of mice and their entrainment to light. The overexpression of SIRT1 protected mice from these age-dependent effects. Similarly, the administration of fat, ketone bodies, or nicotinamide rescued the circadian expression of clock genes in Alzheimer's disease mouse models and restored their locomotor rhythmicity.