Vitamin E and Alzheimer’s disease: the mediating role of cellular aging
Background Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer’s disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects. Aim Since these modifications may modulate the markers...
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| Veröffentlicht in: | Aging clinical and experimental research 2020-03, Vol.32 (3), p.459-464 |
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| creator | Casati, Martina Boccardi, Virginia Ferri, Evelyn Bertagnoli, Laura Bastiani, Patrizia Ciccone, Simona Mansi, Marta Scamosci, Michela Rossi, Paolo Dionigi Mecocci, Patrizia Arosio, Beatrice |
| description | Background
Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer’s disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects.
Aim
Since these modifications may modulate the markers of oxidative stress and cellular aging, we aim to explore the relationship between vitamin E forms and leukocyte telomere length (LTL) in AD.
Methods
53 AD subjects and 40 cognitively healthy controls (CTs) were enrolled. The vitamin E forms (α-, β-, γ- and δ-tocopherol, α-, β-, γ- and δ-tocotrienol), the ratio of α-tocopherylquinone/α-tocopherol and 5-nitro-γ-tocopherol/γ-tocopherol (markers of oxidative/nitrosative damage) and LTL were measured.
Results and discussion
Regression model was used to explore the associations of vitamin E forms and LTL with AD. The interaction of LTL in the association between vitamin E forms and AD was tested. AD subjects showed significantly lower concentrations of α-, β-, γ- and δ-tocopherol, α- and δ-tocotrienol, total tocopherols, total tocotrienols and total vitamin E compared to CTs. AD subjects showed higher values of nitrosative/oxidative damage. The adjusted analyses confirmed a significant relationship of AD with plasma concentrations of α- and β-tocopherols, δ-tocotrienol, total tocopherols, total tocotrienol, total vitamin E and oxidative/nitrosative damage. However, nitrosative damage was significantly associated with AD only in subjects with higher LTL and not in those expressing marked cellular aging.
Conclusions
Our study confirms the role of vitamin E in AD pathology and indicates that nitrosative damage influences the association with AD only in subjects characterized by longer LTL. |
| doi_str_mv | 10.1007/s40520-019-01209-3 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2229230517</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2229230517</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-24e20c13f1f8b243ba3db1d834808932c798c22ce04a3407cb943acf545822c73</originalsourceid><addsrcrecordid>eNp9kLtOwzAUhi0EoqXwAgzIEgtLwMfHVhK2qipQCYkFWC3HcdpUuRQ7GWDiNXg9ngSXlosYGCzbx9_5ffQRcgzsHBiLL7xgkrOIQRoWZ2mEO2QIcSglCOnur_OAHHi_ZExAuOyTAQKTAkAOyeyx7HRdNnRKdZPTcfWysGVt3fvrm6d56a329pJ2C0trm5e6K5s5dW1laVtQY6uqr7Sjeh7Kh2Sv0JW3R9t9RB6upveTm-j27no2Gd9GBmPZRVxYzgxgAUWScYGZxjyDPEGRsCRFbuI0MZwby4RGwWKTpQK1KaSQSSjHOCJnm9yVa5966ztVl349im5s23vFOU85Mglr9PQPumx714TpFMcYYgmASaD4hjKu9d7ZQq1cWWv3rICptWi1Ea2CaPUpWmFoOtlG91kw893yZTYAuAF8eGrm1v38_U_sB-U5hs0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2371751138</pqid></control><display><type>article</type><title>Vitamin E and Alzheimer’s disease: the mediating role of cellular aging</title><source>SpringerLink Journals</source><creator>Casati, Martina ; Boccardi, Virginia ; Ferri, Evelyn ; Bertagnoli, Laura ; Bastiani, Patrizia ; Ciccone, Simona ; Mansi, Marta ; Scamosci, Michela ; Rossi, Paolo Dionigi ; Mecocci, Patrizia ; Arosio, Beatrice</creator><creatorcontrib>Casati, Martina ; Boccardi, Virginia ; Ferri, Evelyn ; Bertagnoli, Laura ; Bastiani, Patrizia ; Ciccone, Simona ; Mansi, Marta ; Scamosci, Michela ; Rossi, Paolo Dionigi ; Mecocci, Patrizia ; Arosio, Beatrice</creatorcontrib><description>Background
Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer’s disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects.
Aim
Since these modifications may modulate the markers of oxidative stress and cellular aging, we aim to explore the relationship between vitamin E forms and leukocyte telomere length (LTL) in AD.
Methods
53 AD subjects and 40 cognitively healthy controls (CTs) were enrolled. The vitamin E forms (α-, β-, γ- and δ-tocopherol, α-, β-, γ- and δ-tocotrienol), the ratio of α-tocopherylquinone/α-tocopherol and 5-nitro-γ-tocopherol/γ-tocopherol (markers of oxidative/nitrosative damage) and LTL were measured.
Results and discussion
Regression model was used to explore the associations of vitamin E forms and LTL with AD. The interaction of LTL in the association between vitamin E forms and AD was tested. AD subjects showed significantly lower concentrations of α-, β-, γ- and δ-tocopherol, α- and δ-tocotrienol, total tocopherols, total tocotrienols and total vitamin E compared to CTs. AD subjects showed higher values of nitrosative/oxidative damage. The adjusted analyses confirmed a significant relationship of AD with plasma concentrations of α- and β-tocopherols, δ-tocotrienol, total tocopherols, total tocotrienol, total vitamin E and oxidative/nitrosative damage. However, nitrosative damage was significantly associated with AD only in subjects with higher LTL and not in those expressing marked cellular aging.
Conclusions
Our study confirms the role of vitamin E in AD pathology and indicates that nitrosative damage influences the association with AD only in subjects characterized by longer LTL.</description><identifier>ISSN: 1720-8319</identifier><identifier>ISSN: 1594-0667</identifier><identifier>EISSN: 1720-8319</identifier><identifier>DOI: 10.1007/s40520-019-01209-3</identifier><identifier>PMID: 31054115</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Aging ; Alzheimer's disease ; Antioxidants ; Dementia ; Deoxyribonucleic acid ; DNA ; Gene expression ; Geriatrics ; Geriatrics/Gerontology ; Medicine ; Medicine & Public Health ; Neurodegeneration ; Original Article ; Oxidative stress ; Signal transduction ; Telomerase ; Thermal cycling ; Vitamin E</subject><ispartof>Aging clinical and experimental research, 2020-03, Vol.32 (3), p.459-464</ispartof><rights>Springer Nature Switzerland AG 2019</rights><rights>Aging Clinical and Experimental Research is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-24e20c13f1f8b243ba3db1d834808932c798c22ce04a3407cb943acf545822c73</citedby><cites>FETCH-LOGICAL-c375t-24e20c13f1f8b243ba3db1d834808932c798c22ce04a3407cb943acf545822c73</cites><orcidid>0000-0002-0615-3580 ; 0000-0002-7423-3793 ; 0000-0003-2134-1122 ; 0000-0003-0729-5246 ; 0000-0002-5447-5576</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/s40520-019-01209-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s40520-019-01209-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31054115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Casati, Martina</creatorcontrib><creatorcontrib>Boccardi, Virginia</creatorcontrib><creatorcontrib>Ferri, Evelyn</creatorcontrib><creatorcontrib>Bertagnoli, Laura</creatorcontrib><creatorcontrib>Bastiani, Patrizia</creatorcontrib><creatorcontrib>Ciccone, Simona</creatorcontrib><creatorcontrib>Mansi, Marta</creatorcontrib><creatorcontrib>Scamosci, Michela</creatorcontrib><creatorcontrib>Rossi, Paolo Dionigi</creatorcontrib><creatorcontrib>Mecocci, Patrizia</creatorcontrib><creatorcontrib>Arosio, Beatrice</creatorcontrib><title>Vitamin E and Alzheimer’s disease: the mediating role of cellular aging</title><title>Aging clinical and experimental research</title><addtitle>Aging Clin Exp Res</addtitle><addtitle>Aging Clin Exp Res</addtitle><description>Background
Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer’s disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects.
Aim
Since these modifications may modulate the markers of oxidative stress and cellular aging, we aim to explore the relationship between vitamin E forms and leukocyte telomere length (LTL) in AD.
Methods
53 AD subjects and 40 cognitively healthy controls (CTs) were enrolled. The vitamin E forms (α-, β-, γ- and δ-tocopherol, α-, β-, γ- and δ-tocotrienol), the ratio of α-tocopherylquinone/α-tocopherol and 5-nitro-γ-tocopherol/γ-tocopherol (markers of oxidative/nitrosative damage) and LTL were measured.
Results and discussion
Regression model was used to explore the associations of vitamin E forms and LTL with AD. The interaction of LTL in the association between vitamin E forms and AD was tested. AD subjects showed significantly lower concentrations of α-, β-, γ- and δ-tocopherol, α- and δ-tocotrienol, total tocopherols, total tocotrienols and total vitamin E compared to CTs. AD subjects showed higher values of nitrosative/oxidative damage. The adjusted analyses confirmed a significant relationship of AD with plasma concentrations of α- and β-tocopherols, δ-tocotrienol, total tocopherols, total tocotrienol, total vitamin E and oxidative/nitrosative damage. However, nitrosative damage was significantly associated with AD only in subjects with higher LTL and not in those expressing marked cellular aging.
Conclusions
Our study confirms the role of vitamin E in AD pathology and indicates that nitrosative damage influences the association with AD only in subjects characterized by longer LTL.</description><subject>Aging</subject><subject>Alzheimer's disease</subject><subject>Antioxidants</subject><subject>Dementia</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene expression</subject><subject>Geriatrics</subject><subject>Geriatrics/Gerontology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurodegeneration</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Signal transduction</subject><subject>Telomerase</subject><subject>Thermal cycling</subject><subject>Vitamin E</subject><issn>1720-8319</issn><issn>1594-0667</issn><issn>1720-8319</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kLtOwzAUhi0EoqXwAgzIEgtLwMfHVhK2qipQCYkFWC3HcdpUuRQ7GWDiNXg9ngSXlosYGCzbx9_5ffQRcgzsHBiLL7xgkrOIQRoWZ2mEO2QIcSglCOnur_OAHHi_ZExAuOyTAQKTAkAOyeyx7HRdNnRKdZPTcfWysGVt3fvrm6d56a329pJ2C0trm5e6K5s5dW1laVtQY6uqr7Sjeh7Kh2Sv0JW3R9t9RB6upveTm-j27no2Gd9GBmPZRVxYzgxgAUWScYGZxjyDPEGRsCRFbuI0MZwby4RGwWKTpQK1KaSQSSjHOCJnm9yVa5966ztVl349im5s23vFOU85Mglr9PQPumx714TpFMcYYgmASaD4hjKu9d7ZQq1cWWv3rICptWi1Ea2CaPUpWmFoOtlG91kw893yZTYAuAF8eGrm1v38_U_sB-U5hs0</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Casati, Martina</creator><creator>Boccardi, Virginia</creator><creator>Ferri, Evelyn</creator><creator>Bertagnoli, Laura</creator><creator>Bastiani, Patrizia</creator><creator>Ciccone, Simona</creator><creator>Mansi, Marta</creator><creator>Scamosci, Michela</creator><creator>Rossi, Paolo Dionigi</creator><creator>Mecocci, Patrizia</creator><creator>Arosio, Beatrice</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0615-3580</orcidid><orcidid>https://orcid.org/0000-0002-7423-3793</orcidid><orcidid>https://orcid.org/0000-0003-2134-1122</orcidid><orcidid>https://orcid.org/0000-0003-0729-5246</orcidid><orcidid>https://orcid.org/0000-0002-5447-5576</orcidid></search><sort><creationdate>20200301</creationdate><title>Vitamin E and Alzheimer’s disease: the mediating role of cellular aging</title><author>Casati, Martina ; Boccardi, Virginia ; Ferri, Evelyn ; Bertagnoli, Laura ; Bastiani, Patrizia ; Ciccone, Simona ; Mansi, Marta ; Scamosci, Michela ; Rossi, Paolo Dionigi ; Mecocci, Patrizia ; Arosio, Beatrice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-24e20c13f1f8b243ba3db1d834808932c798c22ce04a3407cb943acf545822c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Alzheimer's disease</topic><topic>Antioxidants</topic><topic>Dementia</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Gene expression</topic><topic>Geriatrics</topic><topic>Geriatrics/Gerontology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurodegeneration</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Signal transduction</topic><topic>Telomerase</topic><topic>Thermal cycling</topic><topic>Vitamin E</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Casati, Martina</creatorcontrib><creatorcontrib>Boccardi, Virginia</creatorcontrib><creatorcontrib>Ferri, Evelyn</creatorcontrib><creatorcontrib>Bertagnoli, Laura</creatorcontrib><creatorcontrib>Bastiani, Patrizia</creatorcontrib><creatorcontrib>Ciccone, Simona</creatorcontrib><creatorcontrib>Mansi, Marta</creatorcontrib><creatorcontrib>Scamosci, Michela</creatorcontrib><creatorcontrib>Rossi, Paolo Dionigi</creatorcontrib><creatorcontrib>Mecocci, Patrizia</creatorcontrib><creatorcontrib>Arosio, Beatrice</creatorcontrib><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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><jtitle>Aging clinical and experimental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Casati, Martina</au><au>Boccardi, Virginia</au><au>Ferri, Evelyn</au><au>Bertagnoli, Laura</au><au>Bastiani, Patrizia</au><au>Ciccone, Simona</au><au>Mansi, Marta</au><au>Scamosci, Michela</au><au>Rossi, Paolo Dionigi</au><au>Mecocci, Patrizia</au><au>Arosio, Beatrice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin E and Alzheimer’s disease: the mediating role of cellular aging</atitle><jtitle>Aging clinical and experimental research</jtitle><stitle>Aging Clin Exp Res</stitle><addtitle>Aging Clin Exp Res</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>32</volume><issue>3</issue><spage>459</spage><epage>464</epage><pages>459-464</pages><issn>1720-8319</issn><issn>1594-0667</issn><eissn>1720-8319</eissn><abstract>Background
Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer’s disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects.
Aim
Since these modifications may modulate the markers of oxidative stress and cellular aging, we aim to explore the relationship between vitamin E forms and leukocyte telomere length (LTL) in AD.
Methods
53 AD subjects and 40 cognitively healthy controls (CTs) were enrolled. The vitamin E forms (α-, β-, γ- and δ-tocopherol, α-, β-, γ- and δ-tocotrienol), the ratio of α-tocopherylquinone/α-tocopherol and 5-nitro-γ-tocopherol/γ-tocopherol (markers of oxidative/nitrosative damage) and LTL were measured.
Results and discussion
Regression model was used to explore the associations of vitamin E forms and LTL with AD. The interaction of LTL in the association between vitamin E forms and AD was tested. AD subjects showed significantly lower concentrations of α-, β-, γ- and δ-tocopherol, α- and δ-tocotrienol, total tocopherols, total tocotrienols and total vitamin E compared to CTs. AD subjects showed higher values of nitrosative/oxidative damage. The adjusted analyses confirmed a significant relationship of AD with plasma concentrations of α- and β-tocopherols, δ-tocotrienol, total tocopherols, total tocotrienol, total vitamin E and oxidative/nitrosative damage. However, nitrosative damage was significantly associated with AD only in subjects with higher LTL and not in those expressing marked cellular aging.
Conclusions
Our study confirms the role of vitamin E in AD pathology and indicates that nitrosative damage influences the association with AD only in subjects characterized by longer LTL.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>31054115</pmid><doi>10.1007/s40520-019-01209-3</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-0615-3580</orcidid><orcidid>https://orcid.org/0000-0002-7423-3793</orcidid><orcidid>https://orcid.org/0000-0003-2134-1122</orcidid><orcidid>https://orcid.org/0000-0003-0729-5246</orcidid><orcidid>https://orcid.org/0000-0002-5447-5576</orcidid></addata></record> |
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| subjects | Aging Alzheimer's disease Antioxidants Dementia Deoxyribonucleic acid DNA Gene expression Geriatrics Geriatrics/Gerontology Medicine Medicine & Public Health Neurodegeneration Original Article Oxidative stress Signal transduction Telomerase Thermal cycling Vitamin E |
| title | Vitamin E and Alzheimer’s disease: the mediating role of cellular aging |
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