Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model
Summary: Impaired sleep is a common aspect of aging and often precedes the onset of Alzheimer’s disease. Here, we compare the effects of sleep deprivation in young wild-type mice and their APP/PS1 littermates, a murine model of Alzheimer’s disease. After 7 h of sleep deprivation, both genotypes exhi...
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| Language: | English |
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Elsevier
2024-11-01
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| Series: | Cell Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124724013287 |
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| author | Neža Cankar Natalie Beschorner Anastasia Tsopanidou Filippa L. Qvist Ana R. Colaço Mie Andersen Celia Kjaerby Christine Delle Marius Lambert Filip Mundt Pia Weikop Mathias Jucker Matthias Mann Niels Henning Skotte Maiken Nedergaard |
| author_facet | Neža Cankar Natalie Beschorner Anastasia Tsopanidou Filippa L. Qvist Ana R. Colaço Mie Andersen Celia Kjaerby Christine Delle Marius Lambert Filip Mundt Pia Weikop Mathias Jucker Matthias Mann Niels Henning Skotte Maiken Nedergaard |
| author_sort | Neža Cankar |
| collection | DOAJ |
| description | Summary: Impaired sleep is a common aspect of aging and often precedes the onset of Alzheimer’s disease. Here, we compare the effects of sleep deprivation in young wild-type mice and their APP/PS1 littermates, a murine model of Alzheimer’s disease. After 7 h of sleep deprivation, both genotypes exhibit an increase in EEG slow-wave activity. However, only the wild-type mice demonstrate an increase in the power of infraslow norepinephrine oscillations, which are characteristic of healthy non-rapid eye movement sleep. Notably, the APP/PS1 mice fail to enhance norepinephrine oscillations 24 h after sleep deprivation, coinciding with an accumulation of cerebral amyloid-β protein. Proteome analysis of cerebrospinal fluid and extracellular fluid further supports these findings by showing altered protein clearance in APP/PS1 mice. We propose that the suppression of infraslow norepinephrine oscillations following sleep deprivation contributes to increased vulnerability to sleep loss and heightens the risk of developing amyloid pathology in early stages of Alzheimer’s disease. |
| format | Article |
| id | doaj-art-879a38c249f7446eb3ef832e4a2b5bc5 |
| institution | Kabale University |
| issn | 2211-1247 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj-art-879a38c249f7446eb3ef832e4a2b5bc52024-11-15T06:11:44ZengElsevierCell Reports2211-12472024-11-014311114977Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer modelNeža Cankar0Natalie Beschorner1Anastasia Tsopanidou2Filippa L. Qvist3Ana R. Colaço4Mie Andersen5Celia Kjaerby6Christine Delle7Marius Lambert8Filip Mundt9Pia Weikop10Mathias Jucker11Matthias Mann12Niels Henning Skotte13Maiken Nedergaard14Center for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark; Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkNNF Center for Protein Research, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, DenmarkProteomics Research Infrastructure, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkDepartment of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, GermanyNNF Center for Protein Research, Faculty of Health Sciences, University of Copenhagen, Copenhagen, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, DenmarkDepartment of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, GermanyNNF Center for Protein Research, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; Department for Proteomics and Signal Transduction, Max-Planck Institute for Biochemistry, Am Klopferspitz 18, 82152 Martinsried, GermanyNNF Center for Protein Research, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, DenmarkCenter for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark; Center for Translational Neuromedicine, University of Rochester Medical School, Elmwood Avenue 601, Rochester, NY 14642, USA; Corresponding authorSummary: Impaired sleep is a common aspect of aging and often precedes the onset of Alzheimer’s disease. Here, we compare the effects of sleep deprivation in young wild-type mice and their APP/PS1 littermates, a murine model of Alzheimer’s disease. After 7 h of sleep deprivation, both genotypes exhibit an increase in EEG slow-wave activity. However, only the wild-type mice demonstrate an increase in the power of infraslow norepinephrine oscillations, which are characteristic of healthy non-rapid eye movement sleep. Notably, the APP/PS1 mice fail to enhance norepinephrine oscillations 24 h after sleep deprivation, coinciding with an accumulation of cerebral amyloid-β protein. Proteome analysis of cerebrospinal fluid and extracellular fluid further supports these findings by showing altered protein clearance in APP/PS1 mice. We propose that the suppression of infraslow norepinephrine oscillations following sleep deprivation contributes to increased vulnerability to sleep loss and heightens the risk of developing amyloid pathology in early stages of Alzheimer’s disease.http://www.sciencedirect.com/science/article/pii/S2211124724013287CP: Neuroscience |
| spellingShingle | Neža Cankar Natalie Beschorner Anastasia Tsopanidou Filippa L. Qvist Ana R. Colaço Mie Andersen Celia Kjaerby Christine Delle Marius Lambert Filip Mundt Pia Weikop Mathias Jucker Matthias Mann Niels Henning Skotte Maiken Nedergaard Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model Cell Reports CP: Neuroscience |
| title | Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model |
| title_full | Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model |
| title_fullStr | Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model |
| title_full_unstemmed | Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model |
| title_short | Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model |
| title_sort | sleep deprivation leads to non adaptive alterations in sleep microarchitecture and amyloid β accumulation in a murine alzheimer model |
| topic | CP: Neuroscience |
| url | http://www.sciencedirect.com/science/article/pii/S2211124724013287 |
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