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CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease
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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE-Hindawi Access to Research
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199059/ https://www.ncbi.nlm.nih.gov/pubmed/22028968 http://dx.doi.org/10.4061/2011/383091 |
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author | Thome, J. Coogan, A. N. Woods, A. G. Darie, C. C. Häßler, F. |
author_facet | Thome, J. Coogan, A. N. Woods, A. G. Darie, C. C. Häßler, F. |
author_sort | Thome, J. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3199059 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | SAGE-Hindawi Access to Research |
record_format | MEDLINE/PubMed |
spelling | pubmed-31990592011-10-25 CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease Thome, J. Coogan, A. N. Woods, A. G. Darie, C. C. Häßler, F. J Aging Res Review Article 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. SAGE-Hindawi Access to Research 2011 2011-10-18 /pmc/articles/PMC3199059/ /pubmed/22028968 http://dx.doi.org/10.4061/2011/383091 Text en Copyright © 2011 J. Thome et al. https://creativecommons.org/licenses/by/3.0/ 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. |
spellingShingle | Review Article Thome, J. Coogan, A. N. Woods, A. G. Darie, C. C. Häßler, F. CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title | CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title_full | CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title_fullStr | CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title_full_unstemmed | CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title_short | CLOCK Genes and Circadian Rhythmicity in Alzheimer Disease |
title_sort | clock genes and circadian rhythmicity in alzheimer disease |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199059/ https://www.ncbi.nlm.nih.gov/pubmed/22028968 http://dx.doi.org/10.4061/2011/383091 |
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