Chronic Sleep Restriction Induces Aβ Accumulation by Disrupting the Balance of Aβ Production and Clearance in Rats
Amyloid-β (Aβ) plays an important role in Alzheimer’s disease (AD) pathogenesis, and growing evidence has shown that poor sleep quality is one of the risk factors for AD, but the mechanisms of sleep deprivation leading to AD have still not been fully demonstrated. In the present study, we used wild-...
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| Veröffentlicht in: | Neurochemical research 2019-04, Vol.44 (4), p.859-873 |
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| creator | Zhao, Beiyu Liu, Peng Wei, Meng Li, Yanbo Liu, Jie Ma, Louyan Shang, Suhang Jiang, Yu Huo, Kang Wang, Jin Qu, Qiumin |
| description | Amyloid-β (Aβ) plays an important role in Alzheimer’s disease (AD) pathogenesis, and growing evidence has shown that poor sleep quality is one of the risk factors for AD, but the mechanisms of sleep deprivation leading to AD have still not been fully demonstrated. In the present study, we used wild-type (WT) rats to determine the effects of chronic sleep restriction (CSR) on Aβ accumulation. We found that CSR-21d rats had learning and memory functional decline in the Morris water maze (MWM) test. Meanwhile, Aβ
42
deposition in the hippocampus and the prefrontal cortex was high after a 21-day sleep restriction. Moreover, compared with the control rats, CSR rats had increased expression of β-site APP-cleaving enzyme 1 (BACE1) and sAPPβ and decreased sAPPα levels in both the hippocampus and the prefrontal cortex, and the BACE1 level was positively correlated with the Aβ
42
level. Additionally, in CSR-21d rats, low-density lipoprotein receptor-related protein 1 (LRP-1) levels were low, while receptor of advanced glycation end products (RAGE) levels were high in the hippocampus and the prefrontal cortex, and these transporters were significantly correlated with Aβ
42
levels. In addition, CSR-21d rats had decreased plasma Aβ
42
levels and soluble LRP1 (sLRP1) levels compared with the control rats. Altogether, this study demonstrated that 21 days of CSR could lead to brain Aβ accumulation in WT rats. The underlying mechanisms may be related to increased Aβ production via upregulation of the BACE1 pathway and disrupted Aβ clearance affecting brain and peripheral Aβ transport. |
| doi_str_mv | 10.1007/s11064-019-02719-2 |
| format | Article |
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42
deposition in the hippocampus and the prefrontal cortex was high after a 21-day sleep restriction. Moreover, compared with the control rats, CSR rats had increased expression of β-site APP-cleaving enzyme 1 (BACE1) and sAPPβ and decreased sAPPα levels in both the hippocampus and the prefrontal cortex, and the BACE1 level was positively correlated with the Aβ
42
level. Additionally, in CSR-21d rats, low-density lipoprotein receptor-related protein 1 (LRP-1) levels were low, while receptor of advanced glycation end products (RAGE) levels were high in the hippocampus and the prefrontal cortex, and these transporters were significantly correlated with Aβ
42
levels. In addition, CSR-21d rats had decreased plasma Aβ
42
levels and soluble LRP1 (sLRP1) levels compared with the control rats. Altogether, this study demonstrated that 21 days of CSR could lead to brain Aβ accumulation in WT rats. The underlying mechanisms may be related to increased Aβ production via upregulation of the BACE1 pathway and disrupted Aβ clearance affecting brain and peripheral Aβ transport.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-019-02719-2</identifier><identifier>PMID: 30632087</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Accumulation ; Advanced glycosylation end products ; Alzheimer's disease ; Amyloid ; Amyloid beta-Peptides - biosynthesis ; Amyloid beta-Peptides - metabolism ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Cell Biology ; Disruption ; Glycosylation ; Hippocampus ; Hippocampus - metabolism ; Hippocampus - pathology ; Learning ; Male ; Maze learning ; Maze Learning - physiology ; Memory ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Pathogenesis ; Peptide Fragments - biosynthesis ; Peptide Fragments - metabolism ; Prefrontal cortex ; Prefrontal Cortex - metabolism ; Prefrontal Cortex - pathology ; Proteins ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor density ; Risk analysis ; Risk factors ; Rodents ; Sleep ; Sleep deprivation ; Sleep Deprivation - complications ; Sleep Deprivation - metabolism ; Sleep Deprivation - pathology ; β-Site APP-cleaving enzyme 1</subject><ispartof>Neurochemical research, 2019-04, Vol.44 (4), p.859-873</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Neurochemical Research is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2902-b42c9a137714ff3101d4282907c134c66146b2a5d7ac8e43dd2efb71190d41e63</citedby><cites>FETCH-LOGICAL-c2902-b42c9a137714ff3101d4282907c134c66146b2a5d7ac8e43dd2efb71190d41e63</cites><orcidid>0000-0002-7246-0896</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-019-02719-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-019-02719-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30632087$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Beiyu</creatorcontrib><creatorcontrib>Liu, Peng</creatorcontrib><creatorcontrib>Wei, Meng</creatorcontrib><creatorcontrib>Li, Yanbo</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Ma, Louyan</creatorcontrib><creatorcontrib>Shang, Suhang</creatorcontrib><creatorcontrib>Jiang, Yu</creatorcontrib><creatorcontrib>Huo, Kang</creatorcontrib><creatorcontrib>Wang, Jin</creatorcontrib><creatorcontrib>Qu, Qiumin</creatorcontrib><title>Chronic Sleep Restriction Induces Aβ Accumulation by Disrupting the Balance of Aβ Production and Clearance in Rats</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Amyloid-β (Aβ) plays an important role in Alzheimer’s disease (AD) pathogenesis, and growing evidence has shown that poor sleep quality is one of the risk factors for AD, but the mechanisms of sleep deprivation leading to AD have still not been fully demonstrated. In the present study, we used wild-type (WT) rats to determine the effects of chronic sleep restriction (CSR) on Aβ accumulation. We found that CSR-21d rats had learning and memory functional decline in the Morris water maze (MWM) test. Meanwhile, Aβ
42
deposition in the hippocampus and the prefrontal cortex was high after a 21-day sleep restriction. Moreover, compared with the control rats, CSR rats had increased expression of β-site APP-cleaving enzyme 1 (BACE1) and sAPPβ and decreased sAPPα levels in both the hippocampus and the prefrontal cortex, and the BACE1 level was positively correlated with the Aβ
42
level. Additionally, in CSR-21d rats, low-density lipoprotein receptor-related protein 1 (LRP-1) levels were low, while receptor of advanced glycation end products (RAGE) levels were high in the hippocampus and the prefrontal cortex, and these transporters were significantly correlated with Aβ
42
levels. In addition, CSR-21d rats had decreased plasma Aβ
42
levels and soluble LRP1 (sLRP1) levels compared with the control rats. Altogether, this study demonstrated that 21 days of CSR could lead to brain Aβ accumulation in WT rats. The underlying mechanisms may be related to increased Aβ production via upregulation of the BACE1 pathway and disrupted Aβ clearance affecting brain and peripheral Aβ transport.</description><subject>Accumulation</subject><subject>Advanced glycosylation end products</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Amyloid beta-Peptides - biosynthesis</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Cell Biology</subject><subject>Disruption</subject><subject>Glycosylation</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Learning</subject><subject>Male</subject><subject>Maze learning</subject><subject>Maze Learning - physiology</subject><subject>Memory</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Pathogenesis</subject><subject>Peptide Fragments - biosynthesis</subject><subject>Peptide Fragments - metabolism</subject><subject>Prefrontal cortex</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Prefrontal Cortex - pathology</subject><subject>Proteins</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor density</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Sleep</subject><subject>Sleep deprivation</subject><subject>Sleep Deprivation - complications</subject><subject>Sleep Deprivation - metabolism</subject><subject>Sleep Deprivation - pathology</subject><subject>β-Site APP-cleaving enzyme 1</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kb1OwzAUhS0EglJ4AQZkiYUl4Gs7djOW8lcJCVRgthzHKalSp9jJwGvxIDwTJi0gMbD4Duc7x_fqIHQE5AwIkecBgAieEMgSQmV86RYaQCpZIjLCttGAsCgzyMge2g9hQUi0UdhFe4wIRslIDlA7efGNqwx-rK1d4ZkNra9MWzUOT13RGRvw-OMdj43pll2teyF_w5dV8N2qrdwcty8WX-haO2NxU_b0g2-itWe1K_Ckttr3euXwTLfhAO2Uug72cDOH6Pn66mlym9zd30wn47vE0IzQJOfUZBqYlMDLkgGBgtNRlKQBxo0QwEVOdVpIbUaWs6KgtswlxIMLDlawITpd565889rF09SyCsbWcVnbdEFRkBljPKUsoid_0EXTeRe3i5RIM0FT9hVI15TxTQjelmrlq6X2bwqI-upErTtRsRPVd6JoNB1vort8aYsfy3cJEWBrIETJza3__fuf2E-ToJbZ</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Zhao, Beiyu</creator><creator>Liu, Peng</creator><creator>Wei, Meng</creator><creator>Li, Yanbo</creator><creator>Liu, Jie</creator><creator>Ma, Louyan</creator><creator>Shang, Suhang</creator><creator>Jiang, Yu</creator><creator>Huo, Kang</creator><creator>Wang, Jin</creator><creator>Qu, Qiumin</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7246-0896</orcidid></search><sort><creationdate>20190401</creationdate><title>Chronic Sleep Restriction Induces Aβ Accumulation by Disrupting the Balance of Aβ Production and Clearance in Rats</title><author>Zhao, Beiyu ; Liu, Peng ; Wei, Meng ; Li, Yanbo ; Liu, Jie ; Ma, Louyan ; Shang, Suhang ; Jiang, Yu ; Huo, Kang ; Wang, Jin ; Qu, Qiumin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2902-b42c9a137714ff3101d4282907c134c66146b2a5d7ac8e43dd2efb71190d41e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Accumulation</topic><topic>Advanced glycosylation end products</topic><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Amyloid beta-Peptides - biosynthesis</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Cell Biology</topic><topic>Disruption</topic><topic>Glycosylation</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Learning</topic><topic>Male</topic><topic>Maze learning</topic><topic>Maze Learning - physiology</topic><topic>Memory</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Pathogenesis</topic><topic>Peptide Fragments - biosynthesis</topic><topic>Peptide Fragments - metabolism</topic><topic>Prefrontal cortex</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Prefrontal Cortex - pathology</topic><topic>Proteins</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor density</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>Sleep</topic><topic>Sleep deprivation</topic><topic>Sleep Deprivation - 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Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Beiyu</au><au>Liu, Peng</au><au>Wei, Meng</au><au>Li, Yanbo</au><au>Liu, Jie</au><au>Ma, Louyan</au><au>Shang, Suhang</au><au>Jiang, Yu</au><au>Huo, Kang</au><au>Wang, Jin</au><au>Qu, Qiumin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Sleep Restriction Induces Aβ Accumulation by Disrupting the Balance of Aβ Production and Clearance in Rats</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>44</volume><issue>4</issue><spage>859</spage><epage>873</epage><pages>859-873</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Amyloid-β (Aβ) plays an important role in Alzheimer’s disease (AD) pathogenesis, and growing evidence has shown that poor sleep quality is one of the risk factors for AD, but the mechanisms of sleep deprivation leading to AD have still not been fully demonstrated. In the present study, we used wild-type (WT) rats to determine the effects of chronic sleep restriction (CSR) on Aβ accumulation. We found that CSR-21d rats had learning and memory functional decline in the Morris water maze (MWM) test. Meanwhile, Aβ
42
deposition in the hippocampus and the prefrontal cortex was high after a 21-day sleep restriction. Moreover, compared with the control rats, CSR rats had increased expression of β-site APP-cleaving enzyme 1 (BACE1) and sAPPβ and decreased sAPPα levels in both the hippocampus and the prefrontal cortex, and the BACE1 level was positively correlated with the Aβ
42
level. Additionally, in CSR-21d rats, low-density lipoprotein receptor-related protein 1 (LRP-1) levels were low, while receptor of advanced glycation end products (RAGE) levels were high in the hippocampus and the prefrontal cortex, and these transporters were significantly correlated with Aβ
42
levels. In addition, CSR-21d rats had decreased plasma Aβ
42
levels and soluble LRP1 (sLRP1) levels compared with the control rats. Altogether, this study demonstrated that 21 days of CSR could lead to brain Aβ accumulation in WT rats. The underlying mechanisms may be related to increased Aβ production via upregulation of the BACE1 pathway and disrupted Aβ clearance affecting brain and peripheral Aβ transport.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30632087</pmid><doi>10.1007/s11064-019-02719-2</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-7246-0896</orcidid></addata></record> |
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| ispartof | Neurochemical research, 2019-04, Vol.44 (4), p.859-873 |
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| subjects | Accumulation Advanced glycosylation end products Alzheimer's disease Amyloid Amyloid beta-Peptides - biosynthesis Amyloid beta-Peptides - metabolism Animals Biochemistry Biomedical and Life Sciences Biomedicine Brain Cell Biology Disruption Glycosylation Hippocampus Hippocampus - metabolism Hippocampus - pathology Learning Male Maze learning Maze Learning - physiology Memory Neurochemistry Neurology Neurosciences Original Paper Pathogenesis Peptide Fragments - biosynthesis Peptide Fragments - metabolism Prefrontal cortex Prefrontal Cortex - metabolism Prefrontal Cortex - pathology Proteins Random Allocation Rats Rats, Sprague-Dawley Receptor density Risk analysis Risk factors Rodents Sleep Sleep deprivation Sleep Deprivation - complications Sleep Deprivation - metabolism Sleep Deprivation - pathology β-Site APP-cleaving enzyme 1 |
| title | Chronic Sleep Restriction Induces Aβ Accumulation by Disrupting the Balance of Aβ Production and Clearance in Rats |
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