Effect of the inhaled anesthetics isoflurane, sevoflurane and desflurane on the neuropathogenesis of Alzheimer's disease (Review)
The incidence of Alzheimer's disease (AD) in individuals >65 years of age is 13% and ~66 million individuals in this age group undergo surgery annually under anesthesia. It is therefore important to determine whether commonly used inhaled anesthetics induce cytotoxicity, which may lead to ne...
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| Veröffentlicht in: | Molecular medicine reports 2015-07, Vol.12 (1), p.3-12 |
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| description | The incidence of Alzheimer's disease (AD) in individuals >65 years of age is 13% and ~66 million individuals in this age group undergo surgery annually under anesthesia. It is therefore important to determine whether commonly used inhaled anesthetics induce cytotoxicity, which may lead to neurodegeneration. Findings from several studies suggest that the anesthetics, isoflurane, sevoflurane and desflurane, may activate caspases, increase the synthesis and accumulation of β-amyloid (Aβ) protein, and induce hyperphosphorylation of tau proteins, all of which are cellular responses consistent with the neuropathogenesis of AD. Other studies have arrived at different and occasionally contradictory conclusions. The present review attempts to resolve this discrepancy by reviewing previous studies, which have investigated the effects of commonly used inhaled anesthetics on the synthesis and accumulation of Aβ, tau pathology and cognitive function. The possible underlying mechanism was also reviewed. However, several aspects of this phenomenon remain to be elucidated. Further studies are required to fully examine anesthesia-induced neurotoxicity and elucidate the effect of inhaled anesthetics on the onset and progression of AD. |
| doi_str_mv | 10.3892/mmr.2015.3424 |
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It is therefore important to determine whether commonly used inhaled anesthetics induce cytotoxicity, which may lead to neurodegeneration. Findings from several studies suggest that the anesthetics, isoflurane, sevoflurane and desflurane, may activate caspases, increase the synthesis and accumulation of β-amyloid (Aβ) protein, and induce hyperphosphorylation of tau proteins, all of which are cellular responses consistent with the neuropathogenesis of AD. Other studies have arrived at different and occasionally contradictory conclusions. The present review attempts to resolve this discrepancy by reviewing previous studies, which have investigated the effects of commonly used inhaled anesthetics on the synthesis and accumulation of Aβ, tau pathology and cognitive function. The possible underlying mechanism was also reviewed. However, several aspects of this phenomenon remain to be elucidated. Further studies are required to fully examine anesthesia-induced neurotoxicity and elucidate the effect of inhaled anesthetics on the onset and progression of AD.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2015.3424</identifier><identifier>PMID: 25738734</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Anesthesia ; Anesthetics ; Anesthetics, Inhalation - adverse effects ; Anesthetics, Inhalation - therapeutic use ; Apolipoproteins ; Brain ; Care and treatment ; Caspases - metabolism ; Cognition - drug effects ; Cognitive ability ; cognitive deficits ; Cytotoxicity ; Desflurane ; Development and progression ; Enzymes ; Health aspects ; Humans ; Isoflurane ; Isoflurane - adverse effects ; Isoflurane - analogs & derivatives ; Metabolism ; Metabolites ; Methyl Ethers - adverse effects ; Methyl Ethers - therapeutic use ; Mutation ; Neurodegeneration ; Neurodegenerative diseases ; Neuropathogenesis ; Neuropathology ; Neurotoxicity ; Pathology ; Peptides ; Phosphorylation ; Proteins ; Reviews ; Sevoflurane ; Studies ; Surgery ; tau ; Tau protein ; tau Proteins - metabolism ; β-Amyloid ; β-amyloid protein</subject><ispartof>Molecular medicine reports, 2015-07, Vol.12 (1), p.3-12</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><rights>Copyright © 2015, Spandidos Publications 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-950274d206d1807baff125785d5d768ef5f9490418157bd46e16bcbb63a2d8dd3</citedby><cites>FETCH-LOGICAL-c541t-950274d206d1807baff125785d5d768ef5f9490418157bd46e16bcbb63a2d8dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25738734$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JIANG, JUE</creatorcontrib><creatorcontrib>JIANG, HONG</creatorcontrib><title>Effect of the inhaled anesthetics isoflurane, sevoflurane and desflurane on the neuropathogenesis of Alzheimer's disease (Review)</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>The incidence of Alzheimer's disease (AD) in individuals >65 years of age is 13% and ~66 million individuals in this age group undergo surgery annually under anesthesia. It is therefore important to determine whether commonly used inhaled anesthetics induce cytotoxicity, which may lead to neurodegeneration. Findings from several studies suggest that the anesthetics, isoflurane, sevoflurane and desflurane, may activate caspases, increase the synthesis and accumulation of β-amyloid (Aβ) protein, and induce hyperphosphorylation of tau proteins, all of which are cellular responses consistent with the neuropathogenesis of AD. Other studies have arrived at different and occasionally contradictory conclusions. The present review attempts to resolve this discrepancy by reviewing previous studies, which have investigated the effects of commonly used inhaled anesthetics on the synthesis and accumulation of Aβ, tau pathology and cognitive function. The possible underlying mechanism was also reviewed. However, several aspects of this phenomenon remain to be elucidated. Further studies are required to fully examine anesthesia-induced neurotoxicity and elucidate the effect of inhaled anesthetics on the onset and progression of AD.</description><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Anesthesia</subject><subject>Anesthetics</subject><subject>Anesthetics, Inhalation - adverse effects</subject><subject>Anesthetics, Inhalation - therapeutic use</subject><subject>Apolipoproteins</subject><subject>Brain</subject><subject>Care and treatment</subject><subject>Caspases - metabolism</subject><subject>Cognition - drug effects</subject><subject>Cognitive ability</subject><subject>cognitive deficits</subject><subject>Cytotoxicity</subject><subject>Desflurane</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Isoflurane</subject><subject>Isoflurane - adverse effects</subject><subject>Isoflurane - analogs & derivatives</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Methyl Ethers - adverse effects</subject><subject>Methyl Ethers - therapeutic use</subject><subject>Mutation</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neuropathogenesis</subject><subject>Neuropathology</subject><subject>Neurotoxicity</subject><subject>Pathology</subject><subject>Peptides</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Reviews</subject><subject>Sevoflurane</subject><subject>Studies</subject><subject>Surgery</subject><subject>tau</subject><subject>Tau protein</subject><subject>tau Proteins - metabolism</subject><subject>β-Amyloid</subject><subject>β-amyloid protein</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpVkU2L1TAUhoMozji6dCsBF6Ngr_lsm41wGUYdGBBE1yFtTm4ztM01aa-Mu_nnpt4PnFVykoeHc86L0GtKVrxW7OMwxBUjVK64YOIJOqeVogUnRDw93JlS1Rl6kdIdIaVkUj1HZ0xWvK64OEcP185BO-Hg8NQB9mNnerDYjJByPfk2YZ-C6-eYnz7gBLtjkRmLLaRjGcZ_hhHmGLZm6sIGssSnRb3u_3TgB4iXCVufwCTA777DzsPv9y_RM2f6BK8O5wX6-fn6x9XX4vbbl5ur9W3RSkGnQknCKmEZKS2tSdUY52geo5ZW2qqswUmnhCKC1lRWjRUl0LJpm6bkhtnaWn6BPu2927kZwLYwTtH0ehv9YOK9Dsbrxz-j7_Qm7LQQedGSZMHbgyCGX3Pej74Lcxxzz5oqzkSpREZP1CYvUvvRhSxrB59avRaMy5LTeqGKPdXGkFIEd-qDEr3kqnOueslVL7lm_s3_zZ_oY5AZuNwDaZtz8TakE5NNBWUFoQUhhPO_jlutCQ</recordid><startdate>20150701</startdate><enddate>20150701</enddate><creator>JIANG, JUE</creator><creator>JIANG, HONG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20150701</creationdate><title>Effect of the inhaled anesthetics isoflurane, sevoflurane and desflurane on the neuropathogenesis of Alzheimer's disease (Review)</title><author>JIANG, JUE ; JIANG, HONG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-950274d206d1807baff125785d5d768ef5f9490418157bd46e16bcbb63a2d8dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Anesthesia</topic><topic>Anesthetics</topic><topic>Anesthetics, Inhalation - adverse effects</topic><topic>Anesthetics, Inhalation - therapeutic use</topic><topic>Apolipoproteins</topic><topic>Brain</topic><topic>Care and treatment</topic><topic>Caspases - metabolism</topic><topic>Cognition - drug effects</topic><topic>Cognitive ability</topic><topic>cognitive deficits</topic><topic>Cytotoxicity</topic><topic>Desflurane</topic><topic>Development and progression</topic><topic>Enzymes</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Isoflurane</topic><topic>Isoflurane - adverse effects</topic><topic>Isoflurane - analogs & derivatives</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Methyl Ethers - adverse effects</topic><topic>Methyl Ethers - therapeutic use</topic><topic>Mutation</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neuropathogenesis</topic><topic>Neuropathology</topic><topic>Neurotoxicity</topic><topic>Pathology</topic><topic>Peptides</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Reviews</topic><topic>Sevoflurane</topic><topic>Studies</topic><topic>Surgery</topic><topic>tau</topic><topic>Tau protein</topic><topic>tau Proteins - metabolism</topic><topic>β-Amyloid</topic><topic>β-amyloid protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JIANG, JUE</creatorcontrib><creatorcontrib>JIANG, HONG</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JIANG, JUE</au><au>JIANG, HONG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of the inhaled anesthetics isoflurane, sevoflurane and desflurane on the neuropathogenesis of Alzheimer's disease (Review)</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-07-01</date><risdate>2015</risdate><volume>12</volume><issue>1</issue><spage>3</spage><epage>12</epage><pages>3-12</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The incidence of Alzheimer's disease (AD) in individuals >65 years of age is 13% and ~66 million individuals in this age group undergo surgery annually under anesthesia. It is therefore important to determine whether commonly used inhaled anesthetics induce cytotoxicity, which may lead to neurodegeneration. Findings from several studies suggest that the anesthetics, isoflurane, sevoflurane and desflurane, may activate caspases, increase the synthesis and accumulation of β-amyloid (Aβ) protein, and induce hyperphosphorylation of tau proteins, all of which are cellular responses consistent with the neuropathogenesis of AD. Other studies have arrived at different and occasionally contradictory conclusions. The present review attempts to resolve this discrepancy by reviewing previous studies, which have investigated the effects of commonly used inhaled anesthetics on the synthesis and accumulation of Aβ, tau pathology and cognitive function. The possible underlying mechanism was also reviewed. However, several aspects of this phenomenon remain to be elucidated. Further studies are required to fully examine anesthesia-induced neurotoxicity and elucidate the effect of inhaled anesthetics on the onset and progression of AD.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25738734</pmid><doi>10.3892/mmr.2015.3424</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Amyloid beta-Peptides - metabolism Anesthesia Anesthetics Anesthetics, Inhalation - adverse effects Anesthetics, Inhalation - therapeutic use Apolipoproteins Brain Care and treatment Caspases - metabolism Cognition - drug effects Cognitive ability cognitive deficits Cytotoxicity Desflurane Development and progression Enzymes Health aspects Humans Isoflurane Isoflurane - adverse effects Isoflurane - analogs & derivatives Metabolism Metabolites Methyl Ethers - adverse effects Methyl Ethers - therapeutic use Mutation Neurodegeneration Neurodegenerative diseases Neuropathogenesis Neuropathology Neurotoxicity Pathology Peptides Phosphorylation Proteins Reviews Sevoflurane Studies Surgery tau Tau protein tau Proteins - metabolism β-Amyloid β-amyloid protein |
| title | Effect of the inhaled anesthetics isoflurane, sevoflurane and desflurane on the neuropathogenesis of Alzheimer's disease (Review) |
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