The effect and mechanism of patchouli alcohol on cognitive dysfunction in AD mice induced by Aβ 1-42 oligomers through AMPK/mTOR pathway
Alzheimer's disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic...
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Veröffentlicht in: | Brain research bulletin 2024-09, Vol.215, p.111030 |
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description | Alzheimer's disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic effect of PA on AD using an Aβ
induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ
-induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction. |
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induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ
-induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction.</description><identifier>EISSN: 1873-2747</identifier><identifier>PMID: 38996935</identifier><language>eng</language><publisher>United States</publisher><subject>Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; AMP-Activated Protein Kinases - metabolism ; Amyloid beta-Peptides - metabolism ; Animals ; Cognitive Dysfunction - drug therapy ; Cognitive Dysfunction - metabolism ; Disease Models, Animal ; Male ; Mice ; Microglia - drug effects ; Microglia - metabolism ; Peptide Fragments - metabolism ; Peptide Fragments - toxicity ; Signal Transduction - drug effects ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>Brain research bulletin, 2024-09, Vol.215, p.111030</ispartof><rights>Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38996935$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Li-Ting</creatorcontrib><creatorcontrib>Zhang, Shu-Ting</creatorcontrib><creatorcontrib>Shang, Bao-Ling</creatorcontrib><creatorcontrib>Dai, Yu-Qiong</creatorcontrib><creatorcontrib>Cheng, Xiao-Qing</creatorcontrib><creatorcontrib>Wu, Qing-Guang</creatorcontrib><creatorcontrib>Zhan, Ruo-Ting</creatorcontrib><creatorcontrib>Liu, Si-Jun</creatorcontrib><title>The effect and mechanism of patchouli alcohol on cognitive dysfunction in AD mice induced by Aβ 1-42 oligomers through AMPK/mTOR pathway</title><title>Brain research bulletin</title><addtitle>Brain Res Bull</addtitle><description>Alzheimer's disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic effect of PA on AD using an Aβ
induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ
-induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction.</description><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Cognitive Dysfunction - drug therapy</subject><subject>Cognitive Dysfunction - metabolism</subject><subject>Disease Models, Animal</subject><subject>Male</subject><subject>Mice</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Peptide Fragments - metabolism</subject><subject>Peptide Fragments - toxicity</subject><subject>Signal Transduction - drug effects</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>1873-2747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjltKw0AYhQdBbL1sQf4NBNOmzeUxaEUQUSTvZTrzT-aXuYTMTCVLcDsuxDW1Qn326Rw-DnznjM0XdVVky2pVzdhlCB95npf1urxgs6JumrIp1nP21WkEVApFBO4kWBSaOwoWvIKBR6F9MgTcCK-9Ae9A-N5RpD2CnIJKTkQ6UnLQPoAlgccqk0AJuwnan29YZKsleEO9tzgGiHr0qdfQvrw939nu9f3Xoj_5dM3OFTcBb055xW4fN939UzaknUW5HUayfJy2f9-LfwcHob9Qlg</recordid><startdate>202409</startdate><enddate>202409</enddate><creator>Lin, Li-Ting</creator><creator>Zhang, Shu-Ting</creator><creator>Shang, Bao-Ling</creator><creator>Dai, Yu-Qiong</creator><creator>Cheng, Xiao-Qing</creator><creator>Wu, Qing-Guang</creator><creator>Zhan, Ruo-Ting</creator><creator>Liu, Si-Jun</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>202409</creationdate><title>The effect and mechanism of patchouli alcohol on cognitive dysfunction in AD mice induced by Aβ 1-42 oligomers through AMPK/mTOR pathway</title><author>Lin, Li-Ting ; Zhang, Shu-Ting ; Shang, Bao-Ling ; Dai, Yu-Qiong ; Cheng, Xiao-Qing ; Wu, Qing-Guang ; Zhan, Ruo-Ting ; Liu, Si-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_389969353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Cognitive Dysfunction - drug therapy</topic><topic>Cognitive Dysfunction - metabolism</topic><topic>Disease Models, Animal</topic><topic>Male</topic><topic>Mice</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Peptide Fragments - metabolism</topic><topic>Peptide Fragments - toxicity</topic><topic>Signal Transduction - drug effects</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Li-Ting</creatorcontrib><creatorcontrib>Zhang, Shu-Ting</creatorcontrib><creatorcontrib>Shang, Bao-Ling</creatorcontrib><creatorcontrib>Dai, Yu-Qiong</creatorcontrib><creatorcontrib>Cheng, Xiao-Qing</creatorcontrib><creatorcontrib>Wu, Qing-Guang</creatorcontrib><creatorcontrib>Zhan, Ruo-Ting</creatorcontrib><creatorcontrib>Liu, Si-Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Brain research bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Li-Ting</au><au>Zhang, Shu-Ting</au><au>Shang, Bao-Ling</au><au>Dai, Yu-Qiong</au><au>Cheng, Xiao-Qing</au><au>Wu, Qing-Guang</au><au>Zhan, Ruo-Ting</au><au>Liu, Si-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect and mechanism of patchouli alcohol on cognitive dysfunction in AD mice induced by Aβ 1-42 oligomers through AMPK/mTOR pathway</atitle><jtitle>Brain research bulletin</jtitle><addtitle>Brain Res Bull</addtitle><date>2024-09</date><risdate>2024</risdate><volume>215</volume><spage>111030</spage><pages>111030-</pages><eissn>1873-2747</eissn><abstract>Alzheimer's disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic effect of PA on AD using an Aβ
induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ
-induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction.</abstract><cop>United States</cop><pmid>38996935</pmid></addata></record> |
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subjects | Alzheimer Disease - drug therapy Alzheimer Disease - metabolism AMP-Activated Protein Kinases - metabolism Amyloid beta-Peptides - metabolism Animals Cognitive Dysfunction - drug therapy Cognitive Dysfunction - metabolism Disease Models, Animal Male Mice Microglia - drug effects Microglia - metabolism Peptide Fragments - metabolism Peptide Fragments - toxicity Signal Transduction - drug effects TOR Serine-Threonine Kinases - metabolism |
title | The effect and mechanism of patchouli alcohol on cognitive dysfunction in AD mice induced by Aβ 1-42 oligomers through AMPK/mTOR pathway |
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