Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice?
Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulati...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2021-12-01
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| Series: | Frontiers in Aging Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fnagi.2021.759983/full |
| _version_ | 1818871645957259264 |
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| author | Li Ba Lifang Huang Ziyu He Saiyue Deng Yi Xie Min Zhang Cornelius Jacob Emanuele Antonecchia Emanuele Antonecchia Yuqing Liu Wenchang Xiao Qingguo Xie Qingguo Xie Qingguo Xie Zhili Huang Chenju Yi Nicola D'Ascenzo Nicola D'Ascenzo Fengfei Ding |
| author_facet | Li Ba Lifang Huang Ziyu He Saiyue Deng Yi Xie Min Zhang Cornelius Jacob Emanuele Antonecchia Emanuele Antonecchia Yuqing Liu Wenchang Xiao Qingguo Xie Qingguo Xie Qingguo Xie Zhili Huang Chenju Yi Nicola D'Ascenzo Nicola D'Ascenzo Fengfei Ding |
| author_sort | Li Ba |
| collection | DOAJ |
| description | Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic pre-disposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. 18F-labeled fluorodeoxyglucose positron emission tomography scan (18F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time. |
| first_indexed | 2024-12-19T12:26:13Z |
| format | Article |
| id | doaj.art-0a22b201ecd1481f9359fdb4668bc43c |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-12-19T12:26:13Z |
| publishDate | 2021-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-0a22b201ecd1481f9359fdb4668bc43c2022-12-21T20:21:33ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652021-12-011310.3389/fnagi.2021.759983759983Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice?Li Ba0Lifang Huang1Ziyu He2Saiyue Deng3Yi Xie4Min Zhang5Cornelius Jacob6Emanuele Antonecchia7Emanuele Antonecchia8Yuqing Liu9Wenchang Xiao10Qingguo Xie11Qingguo Xie12Qingguo Xie13Zhili Huang14Chenju Yi15Nicola D'Ascenzo16Nicola D'Ascenzo17Fengfei Ding18Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Medical Physics and Engineering, Istituto Neurologico Mediterraneo Neuromed Istituto di Ricovero e Cura a Carattere Scientifico (I.R.C.C.S.), Pozzilli, ItalyDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Medical Physics and Engineering, Istituto Neurologico Mediterraneo Neuromed Istituto di Ricovero e Cura a Carattere Scientifico (I.R.C.C.S.), Pozzilli, ItalyDepartment of Electronic Engineering and Information Science, University of Science and Technology of China, Hefei, ChinaDepartment of Pharmacology, Shanghai Medical College, Fudan University, Shanghai, ChinaResearch Centre, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, ChinaDepartment of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Medical Physics and Engineering, Istituto Neurologico Mediterraneo Neuromed Istituto di Ricovero e Cura a Carattere Scientifico (I.R.C.C.S.), Pozzilli, ItalyDepartment of Pharmacology, Shanghai Medical College, Fudan University, Shanghai, ChinaChronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic pre-disposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. 18F-labeled fluorodeoxyglucose positron emission tomography scan (18F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time.https://www.frontiersin.org/articles/10.3389/fnagi.2021.759983/fullsleep fragmentationAlzheimer's diseasestressF-18-fluorodeoxyglucose-positron emission tomography (18F-FDG-PET)neuroinflammationtau |
| spellingShingle | Li Ba Lifang Huang Ziyu He Saiyue Deng Yi Xie Min Zhang Cornelius Jacob Emanuele Antonecchia Emanuele Antonecchia Yuqing Liu Wenchang Xiao Qingguo Xie Qingguo Xie Qingguo Xie Zhili Huang Chenju Yi Nicola D'Ascenzo Nicola D'Ascenzo Fengfei Ding Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? Frontiers in Aging Neuroscience sleep fragmentation Alzheimer's disease stress F-18-fluorodeoxyglucose-positron emission tomography (18F-FDG-PET) neuroinflammation tau |
| title | Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? |
| title_full | Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? |
| title_fullStr | Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? |
| title_full_unstemmed | Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? |
| title_short | Does Chronic Sleep Fragmentation Lead to Alzheimer's Disease in Young Wild-Type Mice? |
| title_sort | does chronic sleep fragmentation lead to alzheimer s disease in young wild type mice |
| topic | sleep fragmentation Alzheimer's disease stress F-18-fluorodeoxyglucose-positron emission tomography (18F-FDG-PET) neuroinflammation tau |
| url | https://www.frontiersin.org/articles/10.3389/fnagi.2021.759983/full |
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