Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease
Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain...
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| Veröffentlicht in: | Journal of neuropathology and experimental neurology 1999-07, Vol.58 (7), p.740-747 |
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| container_title | Journal of neuropathology and experimental neurology |
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| creator | Guan, Zhizhong Wang, Yanan Cairns, Nigel J Lantos, Peter L Dallner, Gustav Sindelar, Pavel J |
| description | Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modificationsa significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD. |
| doi_str_mv | 10.1097/00005072-199907000-00008 |
| format | Article |
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To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modificationsa significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/00005072-199907000-00008</identifier><identifier>PMID: 10411344</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Aged ; Aged, 80 and over ; Aldehydes - analysis ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Biological and medical sciences ; Brain ; Brain - metabolism ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA - metabolism ; Fatty Acids - analysis ; Female ; High performance liquid chromatography ; Humans ; Lipids ; Male ; Medical sciences ; Middle Aged ; Monounsaturated fatty acids ; Nerve Tissue Proteins - metabolism ; Neurology ; Phosphatidylcholines - chemistry ; Phosphatidylcholines - metabolism ; Phosphatidylethanolamines - chemistry ; Phosphatidylethanolamines - metabolism ; Phospholipids - metabolism ; Plasmalogens - chemistry ; Plasmalogens - metabolism</subject><ispartof>Journal of neuropathology and experimental neurology, 1999-07, Vol.58 (7), p.740-747</ispartof><rights>1999 American Association of Neuropathologists, Inc</rights><rights>1999 INIST-CNRS</rights><rights>COPYRIGHT 1999 Oxford University Press</rights><rights>Copyright American Association of Neuropathologists, Inc. Jul 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5328-1362229dae12f9c59d50e4dadfa7f36f47fda5a8cf52092405a831fcb1ae181c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1871442$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10411344$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guan, Zhizhong</creatorcontrib><creatorcontrib>Wang, Yanan</creatorcontrib><creatorcontrib>Cairns, Nigel J</creatorcontrib><creatorcontrib>Lantos, Peter L</creatorcontrib><creatorcontrib>Dallner, Gustav</creatorcontrib><creatorcontrib>Sindelar, Pavel J</creatorcontrib><title>Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modificationsa significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aldehydes - analysis</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA - metabolism</subject><subject>Fatty Acids - analysis</subject><subject>Female</subject><subject>High performance liquid chromatography</subject><subject>Humans</subject><subject>Lipids</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Monounsaturated fatty acids</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neurology</subject><subject>Phosphatidylcholines - chemistry</subject><subject>Phosphatidylcholines - metabolism</subject><subject>Phosphatidylethanolamines - chemistry</subject><subject>Phosphatidylethanolamines - metabolism</subject><subject>Phospholipids - metabolism</subject><subject>Plasmalogens - chemistry</subject><subject>Plasmalogens - metabolism</subject><issn>0022-3069</issn><issn>1554-6578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkm9vFCEQxjdGY6_Vr2CIMb7bCiy7Cy_P1qpJjU3U12TKDl0qC1fYzaV-ejnv_BMTI7xgZvJ7hiEPVUUYPWVU9a9oWS3tec2UUrQvWb0ryQfVirWtqLu2lw-rFaWc1w3t1FF1nPNtIRRV4nF1xKhgrBFiVd2do0kIGQmEgXya02LmJYEnH-LgrDMwuxgyiZZcjTFvxpIP9x7nEUL0MLmA5MpDnsDHGwzEBTKPSF4nKNHWzSNZ-28jugkTOXd5d9GT6pEFn_Hp4Typvly8-Xz2rr78-Pb92fqyNm3DZc2ajnOuBkDGrTKtGlqKYoDBQm-bzoreDtCCNLblVHFBS9wwa65ZUUhmmpPq5b7vJsW7BfOsJ5cNeg8B45J1p6RqBO_-CzIlWK-kKODzv8DbuKRQHqHLpJ0Ust9Bp3voBjxqF2ycE5iyB5yciQGtK_V123SsVY2iRSD3ApNizgmt3iQ3QbrXjOqd2_qn2_qX2z9KskifHQZaricc_hDu7S3AiwMA2YC3CYJx-TcneyYEL5jYY9voZ0z5q1-2mPSI4OdR_-uzNd8BEC_Bwg</recordid><startdate>199907</startdate><enddate>199907</enddate><creator>Guan, Zhizhong</creator><creator>Wang, Yanan</creator><creator>Cairns, Nigel J</creator><creator>Lantos, Peter L</creator><creator>Dallner, Gustav</creator><creator>Sindelar, Pavel J</creator><general>American Association of Neuropathologists, Inc</general><general>Lippincott Williams & Wilkins</general><general>Oxford University Press</general><scope>IQODW</scope><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>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>199907</creationdate><title>Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease</title><author>Guan, Zhizhong ; Wang, Yanan ; Cairns, Nigel J ; Lantos, Peter L ; Dallner, Gustav ; Sindelar, Pavel J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5328-1362229dae12f9c59d50e4dadfa7f36f47fda5a8cf52092405a831fcb1ae181c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aldehydes - analysis</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's disease</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>DNA - metabolism</topic><topic>Fatty Acids - analysis</topic><topic>Female</topic><topic>High performance liquid chromatography</topic><topic>Humans</topic><topic>Lipids</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Monounsaturated fatty acids</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neurology</topic><topic>Phosphatidylcholines - chemistry</topic><topic>Phosphatidylcholines - metabolism</topic><topic>Phosphatidylethanolamines - chemistry</topic><topic>Phosphatidylethanolamines - metabolism</topic><topic>Phospholipids - metabolism</topic><topic>Plasmalogens - chemistry</topic><topic>Plasmalogens - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guan, Zhizhong</creatorcontrib><creatorcontrib>Wang, Yanan</creatorcontrib><creatorcontrib>Cairns, Nigel J</creatorcontrib><creatorcontrib>Lantos, Peter L</creatorcontrib><creatorcontrib>Dallner, Gustav</creatorcontrib><creatorcontrib>Sindelar, Pavel J</creatorcontrib><collection>Pascal-Francis</collection><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>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</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>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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science 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 Central Basic</collection><collection>SIRS Editorial</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guan, Zhizhong</au><au>Wang, Yanan</au><au>Cairns, Nigel J</au><au>Lantos, Peter L</au><au>Dallner, Gustav</au><au>Sindelar, Pavel J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>1999-07</date><risdate>1999</risdate><volume>58</volume><issue>7</issue><spage>740</spage><epage>747</epage><pages>740-747</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modificationsa significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>10411344</pmid><doi>10.1097/00005072-199907000-00008</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Aged Aged, 80 and over Aldehydes - analysis Alzheimer Disease - metabolism Alzheimer's disease Biological and medical sciences Brain Brain - metabolism Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA - metabolism Fatty Acids - analysis Female High performance liquid chromatography Humans Lipids Male Medical sciences Middle Aged Monounsaturated fatty acids Nerve Tissue Proteins - metabolism Neurology Phosphatidylcholines - chemistry Phosphatidylcholines - metabolism Phosphatidylethanolamines - chemistry Phosphatidylethanolamines - metabolism Phospholipids - metabolism Plasmalogens - chemistry Plasmalogens - metabolism |
| title | Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease |
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