Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease

Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease

Huntington’s disease (HD) is a progressive neurodegenerative disease marked by psychiatric and motor problems. Recently, these findings have been extended to deficits in sleep and circadian function that can be observed in HD patients and in HD mouse models, with abnormal sleep patterns correlating...

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Main Authors: Oakeshott, Stephen, Balci, Fuat, Filippov, Igor, Murphy, Carol, Port, Russell, Connor, David, Paintdakhi, Ahmad, LeSauter, Joseph, Menalled, Liliana, Ramboz, Sylvie, Kwak, Seung, Howland, David, Silver, Rae, Brunner, Dani
Format: Online
Language:English
Published: Public Library of Science 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072044/
id pubmed-3072044
recordtype oai_dc
spelling pubmed-30720442011-04-07 Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease Oakeshott, Stephen Balci, Fuat Filippov, Igor Murphy, Carol Port, Russell Connor, David Paintdakhi, Ahmad LeSauter, Joseph Menalled, Liliana Ramboz, Sylvie Kwak, Seung Howland, David Silver, Rae Brunner, Dani Huntington Disease Huntington’s disease (HD) is a progressive neurodegenerative disease marked by psychiatric and motor problems. Recently, these findings have been extended to deficits in sleep and circadian function that can be observed in HD patients and in HD mouse models, with abnormal sleep patterns correlating with symptom severity in patients. Here, we studied the behavior of the BAC HD mouse model using an 24/7 automated system; the results indicate significant lengthening of the circadian period in the mutant mice. These results reinforce previous findings in HD models and symptomatic HD patients, indicating that circadian dysfunction is a core feature of HD. Public Library of Science 2011-04-05 /pmc/articles/PMC3072044/ /pubmed/21479110 http://dx.doi.org/10.1371/currents.RRN1225 Text en http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Oakeshott, Stephen
Balci, Fuat
Filippov, Igor
Murphy, Carol
Port, Russell
Connor, David
Paintdakhi, Ahmad
LeSauter, Joseph
Menalled, Liliana
Ramboz, Sylvie
Kwak, Seung
Howland, David
Silver, Rae
Brunner, Dani
spellingShingle Oakeshott, Stephen
Balci, Fuat
Filippov, Igor
Murphy, Carol
Port, Russell
Connor, David
Paintdakhi, Ahmad
LeSauter, Joseph
Menalled, Liliana
Ramboz, Sylvie
Kwak, Seung
Howland, David
Silver, Rae
Brunner, Dani
Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
author_facet Oakeshott, Stephen
Balci, Fuat
Filippov, Igor
Murphy, Carol
Port, Russell
Connor, David
Paintdakhi, Ahmad
LeSauter, Joseph
Menalled, Liliana
Ramboz, Sylvie
Kwak, Seung
Howland, David
Silver, Rae
Brunner, Dani
author_sort Oakeshott, Stephen
title Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
title_short Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
title_full Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
title_fullStr Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
title_full_unstemmed Circadian Abnormalities in Motor Activity in a BAC Transgenic Mouse Model of Huntington’s Disease
title_sort circadian abnormalities in motor activity in a bac transgenic mouse model of huntington’s disease
description Huntington’s disease (HD) is a progressive neurodegenerative disease marked by psychiatric and motor problems. Recently, these findings have been extended to deficits in sleep and circadian function that can be observed in HD patients and in HD mouse models, with abnormal sleep patterns correlating with symptom severity in patients. Here, we studied the behavior of the BAC HD mouse model using an 24/7 automated system; the results indicate significant lengthening of the circadian period in the mutant mice. These results reinforce previous findings in HD models and symptomatic HD patients, indicating that circadian dysfunction is a core feature of HD.
publisher Public Library of Science
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072044/
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