| Records |
| Author |
Wang, H.-B.; Whittaker, D.S.; Truong, D.; Mulji, A.K.; Ghiani, C.A.; Loh, D.H.; Colwell, C.S. |
| Title |
Blue light therapy improves circadian dysfunction as well as motor symptoms in two mouse models of Huntington's disease |
Type |
Journal Article |
| Year |
2017 |
Publication |
Neurobiology of Sleep and Circadian Rhythms |
Abbreviated Journal |
Neurobiology of Sleep and Circadian Rhythms |
| Volume |
2 |
Issue |
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Pages |
39-52 |
| Keywords |
animals; Human Health |
| Abstract |
Patients with Huntington's disease (HD) exhibit movement disorders, psychiatric disturbance and cognitive impairments as the disease progresses. Abnormal sleep/wake cycles are common among HD patients with reports of delayed sleep onset, fatigue during the day, and a delayed pattern of melatonin secretion all of which suggest circadian dysfunction. Mouse models of HD confirm disrupted circadian rhythms with pathophysiology found in the central circadian clock (suprachiasmatic nucleus). Importantly, circadian dysfunction manifests early in disease, even before the classic motor symptoms, in both patients and mouse models. Therefore, we hypothesize that the circadian dysfunction may interact with the disease pathology and exacerbate the HD symptoms. If correct, early intervention may benefit patients and delay disease progression. One test of this hypothesis is to determine whether light therapy designed to strengthen this intrinsic timing system can delay the disease progression in mouse models. Therefore, we determined the impact of blue wavelength-enriched light on two HD models: the BACHD and Q175 mice. Both models received 6 hours of blue-light at the beginning of their daily light cycle for 3 months. After treatment, both genotypes showed improvements in their locomotor activity rhythm without significant change to their sleep behavior. Critically, treated mice of both lines exhibited improved motor performance compared to untreated controls. Focusing on the Q175 genotype, we sought to determine whether the treatment altered signaling pathways in brain regions known to be impacted by HD using NanoString gene expression assays. We found that the expression of several HD relevant markers was altered in the striatum and cortex of the treated mice. Our study demonstrates that strengthening the circadian system can delay the progression of HD in pre-clinical models. This work suggests that lighting conditions should be considered when managing treatment of HD and other neurodegenerative disorders. |
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2451-9944 |
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LoNNe @ kyba @ |
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1626 |
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Joo, E.Y.; Abbott, S.M.; Reid, K.J.; Wu, D.; Kang, J.; Wilson, J.; Zee, P.C. |
| Title |
Timing of light exposure and activity in adults with delayed sleep-wake phase disorder |
Type |
Journal Article |
| Year |
2016 |
Publication |
Sleep Medicine |
Abbreviated Journal |
Sleep Med |
| Volume |
32 |
Issue |
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Pages |
259-265 |
| Keywords |
Human Health |
| Abstract |
OBJECTIVE: To characterize the patterns of light exposure and physical activity level and assess their relationship with sleep quality and depressive symptoms in adults with delayed sleep-wake phase disorder (DSWPD). METHODS: 42 DSWPD (22 female, mean age 34.5 y) and 26 (+/-4 years) age-and-sex-matched controls (12 female, mean age 33.4 y) underwent seven days of light and activity monitoring. RESULTS: Individuals with DSWPD had significantly delayed bed times and wake times, but similar sleep duration compared to controls. Subjective sleep quality (Pittsburgh Sleep Quality Index (PSQI)) was poorer in DSWPDs compared to controls. Those with DSWPD had significantly more activity and light exposure late at night (2:00-4:00) and significantly less activity and light exposure in the morning (8:00-11:00). Total 24 h levels of light and activity were not significantly different between DSWPD and controls. However, the DSWPD group had significantly more light exposure than controls 22 h after waking, during their sleep period. Later light exposure correlated with higher depression scores [Beck Depression Index (BDI)] and poorer sleep quality (PSQI). CONCLUSIONS: The light exposure patterns observed in DSWPD likely contribute to and perpetuate the chronically delayed sleep and wake phase in these patients. In addition, increased light exposure during the sleep period may also contribute to the poor sleep quality and mood disorders that are common in these individuals. |
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Department of Neurology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. Electronic address: p-zee@northwestern.edu |
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English |
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1389-9457 |
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PMID:27964860 |
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no |
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LoNNe @ kyba @ |
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1639 |
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Akacem, L.D.; Wright, K.P.J.; LeBourgeois, M.K. |
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Bedtime and evening light exposure influence circadian timing in preschool-age children: A field study |
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Journal Article |
| Year |
2016 |
Publication |
Neurobiology of Sleep and Circadian Rhythms |
Abbreviated Journal |
Neurobiol Sleep Circadian Rhythms |
| Volume |
1 |
Issue |
2 |
Pages |
27-31 |
| Keywords |
Human Health |
| Abstract |
Light exposure and sleep timing are two factors that influence inter-individual variability in the timing of the human circadian clock. The aim of this study was to quantify the degree to which evening light exposure predicts variance in circadian timing over and above bedtime alone in preschool children. Participants were 21 children ages 4.5-5.0 years (4.7 +/- 0.2 years; 9 females). Children followed their typical sleep schedules for 4 days during which time they wore a wrist actigraph to assess sleep timing and a pendant light meter to measure minute-by-minute illuminance levels in lux. On the 5th day, children participated in an in-home dim-light melatonin onset (DLMO) assessment. Light exposure in the 2 h before bedtime was averaged and aggregated across the 4 nights preceding the DLMO assessment. Mean DLMO and bedtime were 19:22 +/- 01:04 and 20:07 +/- 00:46, respectively. Average evening light exposure was 710.1 +/- 1418.2 lux. Children with later bedtimes (lights-off time) had more delayed melatonin onset times (r=0.61, p=0.002). Evening light exposure was not independently associated with DLMO (r=0.32, p=0.08); however, a partial correlation between evening light exposure and DLMO when controlling for bedtime yielded a positive correlation (r=0.46, p=0.02). Bedtime explained 37.3% of the variance in the timing of DLMO, and evening light exposure accounted for an additional 13.3% of the variance. These findings represent an important step in understanding factors that influence circadian phase in preschool-age children and have implications for understanding a modifiable pathway that may underlie late sleep timing and the development of evening settling problems in early childhood. |
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Sleep and Development Laboratory, Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA |
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English |
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2451-9944 |
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PMID:28042611; PMCID:PMC5193478 |
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LoNNe @ kyba @ |
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1755 |
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