Chronic Fragmentation of the Daily Sleep-Wake Rhythm Increases Amyloid-beta Levels and Neuroinflammation in the 3xTg-AD Mouse Model of Alzheimer's Disease.
Chronic Fragmentation of the Daily Sleep-Wake Rhythm Increases Amyloid-beta Levels and Neuroinflammation in the 3xTg-AD Mouse Model of Alzheimer's Disease.
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DOI：
10.1016/j.neuroscience.2021.11.042
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发表时间：
2022-01-15
期刊：
影响因子：
3.3
通讯作者：
Murphy MP
中科院分区：
文献类型：
--
作者：
Duncan MJ;Guerriero LE;Kohler K;Beechem LE;Gillis BD;Salisbury F;Wessel C;Wang J;Sunderam S;Bachstetter AD;O'Hara BF;Murphy MP
Fragmentation of the daily sleep-wake rhythm with increased nighttime awakenings and more daytime naps is correlated with the risk of development of Alzheimer’s disease (AD). To explore whether a causal relationship underlies this correlation, the present study tested the hypothesis that chronic fragmentation of the daily sleep-wake rhythm stimulates brain amyloid-beta (Aβ) levels and neuroinflammation in the 3xTg-AD mouse model of AD. Female 3xTg-AD mice were allowed to sleep undisturbed or were subjected to chronic sleep fragmentation consisting of four daily sessions of enforced wakefulness (one hour each) evenly distributed during the light phase, five days a week for four weeks. Piezoelectric sleep recording revealed that sleep fragmentation altered the daily sleep-wake rhythm to resemble the pattern observed in AD. Levels of amyloid-beta (Aβ40 and Aβ42) determined by ELISA were higher in hippocampal tissue collected from sleep-fragmented mice than from undisturbed controls. In contrast, hippocampal levels of tau and phospho-tau differed minimally between sleep fragmented and undisturbed control mice. Sleep fragmentation also stimulated neuroinflammation as shown by increased expression of markers of microglial activation and proinflammatory cytokines measured by q-RT-PCR analysis of hippocampal samples. No significant effects of sleep fragmentation on Aβ, tau, or neuroinflammation were observed in the cerebral cortex. These studies support the concept that improving sleep consolidation in individuals at risk for AD may be beneficial for slowing the onset or progression of this devastating neurodegenerative disease.
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影响因子：
3.7
作者：
Bories C;Guitton MJ;Julien C;Tremblay C;Vandal M;Msaid M;De Koninck Y;Calon F
通讯作者：
Calon F
DOI：
10.1016/s2666-7568(20)30015-5
发表时间：
2020-12
期刊：
The lancet. Healthy longevity
影响因子：
--
作者：
Li P;Gao L;Gaba A;Yu L;Cui L;Fan W;Lim ASP;Bennett DA;Buchman AS;Hu K
通讯作者：
Hu K
DOI：
10.1126/science.1180962
发表时间：
2009-11-13
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Kang JE;Lim MM;Bateman RJ;Lee JJ;Smyth LP;Cirrito JR;Fujiki N;Nishino S;Holtzman DM
通讯作者：
Holtzman DM
影响因子：
2.4
作者：
Guarnieri, Biancamaria;Sorbi, Sandro
通讯作者：
Sorbi, Sandro
影响因子：
14.5
作者：
Ju, Yo-El S.;Ooms, Sharon J.;Holtzman, David M.
通讯作者：
Holtzman, David M.