Circadian learning and memory changes in Aβ1–42 induced Alzheimer’s mice
Alzheimer disease (AD) is a growing health problem globally, which causes a progressive decline in learning and memory and multiple disturbances of circadian rhythms. Six Alzheimer’s mice and six wild type (WT) mice were involved in this study. Morris Water Maze (MWM) tasks were conducted hourly to...
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Veröffentlicht in: | Metabolic brain disease 2020-03, Vol.35 (3), p.463-471 |
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description | Alzheimer disease (AD) is a growing health problem globally, which causes a progressive decline in learning and memory and multiple disturbances of circadian rhythms. Six Alzheimer’s mice and six wild type (WT) mice were involved in this study. Morris Water Maze (MWM) tasks were conducted hourly to evaluate their circadian learning and memory performance. We used a single cosinor-based method to evaluate the circadian learning and memory of Alzheimer’s mice and WT mice, respectively. An area sensor was used to record locomotor activity for 2 weeks continuously, including 7 days of 12 h light/12 h dark (LD) conditions and 7 days of 12 h dark/12 h dark (DD) conditions. All WT mice showed circadian rhythm presence in learning and memory, and the peak of escape latency appeared at circadian time (CT) 12. Only one in six Alzheimer’s mice showed a circadian rhythm, but the peak of escape latency was postponed to CT20. Alzheimer’s mice showed rhythm absence under LD or DD conditions. Under LD conditions, the WT mice activity was higher than that in the Alzheimer’s mice during ZT0–5 (
p
= 0.007) and ZT18–23 (
p
= 0.353) but lower during ZT6–11 (
p
|
doi_str_mv | 10.1007/s11011-019-00509-x |
format | Article |
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p
= 0.007) and ZT18–23 (
p
= 0.353) but lower during ZT6–11 (
p
< 0.001) and ZT12–17 (
p
< 0.001). Learning and memory of wild type mice is proved to have a circadian variation throughout a day. In Alzheimer’s mice, rhythmic locomotor activity and circadian learning and memory performance were disrupted. Understanding the role of rhythmic disturbances in the process of AD may assist to identify therapeutic targets.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-019-00509-x</identifier><identifier>PMID: 31728887</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Alzheimer Disease - chemically induced ; Alzheimer Disease - physiopathology ; Alzheimer Disease - psychology ; Alzheimer's disease ; Amyloid beta-Peptides ; Animal memory ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Circadian rhythm ; Circadian Rhythm - physiology ; Circadian rhythms ; Cognitive ability ; Disease Models, Animal ; Disturbances ; Latency ; Learning ; Locomotor activity ; Maze learning ; Maze Learning - physiology ; Memory - physiology ; Metabolic Diseases ; Mice ; Motor Activity - physiology ; Neurodegenerative diseases ; Neurology ; Neurosciences ; Oncology ; Original Article ; Peptide Fragments ; Rodents ; Target recognition ; Therapeutic applications</subject><ispartof>Metabolic brain disease, 2020-03, Vol.35 (3), p.463-471</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Metabolic Brain Disease is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c290x-da98643cace540c15e51e330adcc7ac65aa533aea415e2847cf8dc47d847c3123</citedby><cites>FETCH-LOGICAL-c290x-da98643cace540c15e51e330adcc7ac65aa533aea415e2847cf8dc47d847c3123</cites><orcidid>0000-0002-1342-7762</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/s11011-019-00509-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-019-00509-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31728887$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xuepei</creatorcontrib><creatorcontrib>Guan, Junwen</creatorcontrib><creatorcontrib>Sun, Tong</creatorcontrib><creatorcontrib>Yang, Jingguo</creatorcontrib><creatorcontrib>Yu, Hang</creatorcontrib><creatorcontrib>Yao, Junjie</creatorcontrib><creatorcontrib>Wang, Zhengrong</creatorcontrib><title>Circadian learning and memory changes in Aβ1–42 induced Alzheimer’s mice</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><addtitle>Metab Brain Dis</addtitle><description>Alzheimer disease (AD) is a growing health problem globally, which causes a progressive decline in learning and memory and multiple disturbances of circadian rhythms. Six Alzheimer’s mice and six wild type (WT) mice were involved in this study. Morris Water Maze (MWM) tasks were conducted hourly to evaluate their circadian learning and memory performance. We used a single cosinor-based method to evaluate the circadian learning and memory of Alzheimer’s mice and WT mice, respectively. An area sensor was used to record locomotor activity for 2 weeks continuously, including 7 days of 12 h light/12 h dark (LD) conditions and 7 days of 12 h dark/12 h dark (DD) conditions. All WT mice showed circadian rhythm presence in learning and memory, and the peak of escape latency appeared at circadian time (CT) 12. Only one in six Alzheimer’s mice showed a circadian rhythm, but the peak of escape latency was postponed to CT20. Alzheimer’s mice showed rhythm absence under LD or DD conditions. Under LD conditions, the WT mice activity was higher than that in the Alzheimer’s mice during ZT0–5 (
p
= 0.007) and ZT18–23 (
p
= 0.353) but lower during ZT6–11 (
p
< 0.001) and ZT12–17 (
p
< 0.001). Learning and memory of wild type mice is proved to have a circadian variation throughout a day. In Alzheimer’s mice, rhythmic locomotor activity and circadian learning and memory performance were disrupted. Understanding the role of rhythmic disturbances in the process of AD may assist to identify therapeutic targets.</description><subject>Alzheimer Disease - chemically induced</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer Disease - psychology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides</subject><subject>Animal memory</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Circadian rhythm</subject><subject>Circadian Rhythm - physiology</subject><subject>Circadian rhythms</subject><subject>Cognitive ability</subject><subject>Disease Models, Animal</subject><subject>Disturbances</subject><subject>Latency</subject><subject>Learning</subject><subject>Locomotor activity</subject><subject>Maze learning</subject><subject>Maze Learning - physiology</subject><subject>Memory - physiology</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Motor Activity - physiology</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Peptide Fragments</subject><subject>Rodents</subject><subject>Target recognition</subject><subject>Therapeutic applications</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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>eNp9kE1OwzAQhS0EoqVwARYoEmvDTBzXzrKq-JOK2MDaMrbbpmqSYhOpsOodWHENDsIhehJcUmDHamb03rwnfYQcI5whgDgPiIBIAXMKwCGnyx3SRS4YFazPd0kXpORUZDl0yEEIMwBgHPN90mEoUiml6JLbYeGNtoWukrnTviqqSaIrm5SurP1LYqa6mriQFFUy-PzA9eotS-NhG-NsMpi_Tl1ROr9evYekLIw7JHtjPQ_uaDt75OHy4n54TUd3VzfDwYiaNIcltTqX_YwZbRzPwCB3HB1joK0xQps-15ozpp3OopTKTJixtCYTdrMyTFmPnLa5C18_NS48q1nd-CpWqpQJ5FxyvnGlrcv4OgTvxmrhi1L7F4WgNgRVS1BFguqboFrGp5NtdPNYOvv78oMsGlhrCFGKcPxf9z-xXx06ffk</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Li, Xuepei</creator><creator>Guan, Junwen</creator><creator>Sun, Tong</creator><creator>Yang, Jingguo</creator><creator>Yu, Hang</creator><creator>Yao, Junjie</creator><creator>Wang, Zhengrong</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>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0002-1342-7762</orcidid></search><sort><creationdate>20200301</creationdate><title>Circadian learning and memory changes in Aβ1–42 induced Alzheimer’s mice</title><author>Li, Xuepei ; Guan, Junwen ; Sun, Tong ; Yang, Jingguo ; Yu, Hang ; Yao, Junjie ; Wang, Zhengrong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c290x-da98643cace540c15e51e330adcc7ac65aa533aea415e2847cf8dc47d847c3123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alzheimer Disease - chemically induced</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer Disease - psychology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides</topic><topic>Animal memory</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Circadian rhythm</topic><topic>Circadian Rhythm - physiology</topic><topic>Circadian rhythms</topic><topic>Cognitive ability</topic><topic>Disease Models, Animal</topic><topic>Disturbances</topic><topic>Latency</topic><topic>Learning</topic><topic>Locomotor activity</topic><topic>Maze learning</topic><topic>Maze Learning - physiology</topic><topic>Memory - physiology</topic><topic>Metabolic Diseases</topic><topic>Mice</topic><topic>Motor Activity - physiology</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Peptide Fragments</topic><topic>Rodents</topic><topic>Target recognition</topic><topic>Therapeutic applications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xuepei</creatorcontrib><creatorcontrib>Guan, Junwen</creatorcontrib><creatorcontrib>Sun, Tong</creatorcontrib><creatorcontrib>Yang, Jingguo</creatorcontrib><creatorcontrib>Yu, Hang</creatorcontrib><creatorcontrib>Yao, Junjie</creatorcontrib><creatorcontrib>Wang, Zhengrong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xuepei</au><au>Guan, Junwen</au><au>Sun, Tong</au><au>Yang, Jingguo</au><au>Yu, Hang</au><au>Yao, Junjie</au><au>Wang, Zhengrong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circadian learning and memory changes in Aβ1–42 induced Alzheimer’s mice</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>35</volume><issue>3</issue><spage>463</spage><epage>471</epage><pages>463-471</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>Alzheimer disease (AD) is a growing health problem globally, which causes a progressive decline in learning and memory and multiple disturbances of circadian rhythms. Six Alzheimer’s mice and six wild type (WT) mice were involved in this study. Morris Water Maze (MWM) tasks were conducted hourly to evaluate their circadian learning and memory performance. We used a single cosinor-based method to evaluate the circadian learning and memory of Alzheimer’s mice and WT mice, respectively. An area sensor was used to record locomotor activity for 2 weeks continuously, including 7 days of 12 h light/12 h dark (LD) conditions and 7 days of 12 h dark/12 h dark (DD) conditions. All WT mice showed circadian rhythm presence in learning and memory, and the peak of escape latency appeared at circadian time (CT) 12. Only one in six Alzheimer’s mice showed a circadian rhythm, but the peak of escape latency was postponed to CT20. Alzheimer’s mice showed rhythm absence under LD or DD conditions. Under LD conditions, the WT mice activity was higher than that in the Alzheimer’s mice during ZT0–5 (
p
= 0.007) and ZT18–23 (
p
= 0.353) but lower during ZT6–11 (
p
< 0.001) and ZT12–17 (
p
< 0.001). Learning and memory of wild type mice is proved to have a circadian variation throughout a day. In Alzheimer’s mice, rhythmic locomotor activity and circadian learning and memory performance were disrupted. Understanding the role of rhythmic disturbances in the process of AD may assist to identify therapeutic targets.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31728887</pmid><doi>10.1007/s11011-019-00509-x</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-1342-7762</orcidid></addata></record> |
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subjects | Alzheimer Disease - chemically induced Alzheimer Disease - physiopathology Alzheimer Disease - psychology Alzheimer's disease Amyloid beta-Peptides Animal memory Animals Biochemistry Biomedical and Life Sciences Biomedicine Circadian rhythm Circadian Rhythm - physiology Circadian rhythms Cognitive ability Disease Models, Animal Disturbances Latency Learning Locomotor activity Maze learning Maze Learning - physiology Memory - physiology Metabolic Diseases Mice Motor Activity - physiology Neurodegenerative diseases Neurology Neurosciences Oncology Original Article Peptide Fragments Rodents Target recognition Therapeutic applications |
title | Circadian learning and memory changes in Aβ1–42 induced Alzheimer’s mice |
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