Changes in oxidative damage, inflammation and [NAD(H)] with age in cerebrospinal fluid
An extensive body of evidence indicates that oxidative stress and inflammation play a central role in the degenerative changes of systemic tissues in aging. However a comparatively limited amount of data is available to verify whether these processes also contribute to normal aging within the brain....
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| description | An extensive body of evidence indicates that oxidative stress and inflammation play a central role in the degenerative changes of systemic tissues in aging. However a comparatively limited amount of data is available to verify whether these processes also contribute to normal aging within the brain. High levels of oxidative damage results in key cellular changes including a reduction in available nicotinamide adenine dinucleotide (NAD(+)), an essential molecule required for a number of vital cellular processes including DNA repair, immune signaling and epigenetic processing. In this study we quantified changes in [NAD(H)] and markers of inflammation and oxidative damage (F2-isoprostanes, 8-OHdG, total antioxidant capacity) in the cerebrospinal fluid (CSF) of healthy humans across a wide age range (24-91 years). CSF was collected from consenting patients who required a spinal tap for the administration of anesthetic. CSF of participants aged >45 years was found to contain increased levels of lipid peroxidation (F2-isoprostanes) (p = 0.04) and inflammation (IL-6) (p = 0.00) and decreased levels of both total antioxidant capacity (p = 0.00) and NAD(H) (p = 0.05), compared to their younger counterparts. A positive association was also observed between plasma [NAD(H)] and CSF NAD(H) levels (p = 0.03). Further analysis of the data identified a relationship between alcohol intake and CSF [NAD(H)] and markers of inflammation. The CSF of participants who consumed >1 standard drink of alcohol per day contained lower levels of NAD(H) compared to those who consumed no alcohol (p0-1 (p1 (p |
| doi_str_mv | 10.1371/journal.pone.0085335 |
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However a comparatively limited amount of data is available to verify whether these processes also contribute to normal aging within the brain. High levels of oxidative damage results in key cellular changes including a reduction in available nicotinamide adenine dinucleotide (NAD(+)), an essential molecule required for a number of vital cellular processes including DNA repair, immune signaling and epigenetic processing. In this study we quantified changes in [NAD(H)] and markers of inflammation and oxidative damage (F2-isoprostanes, 8-OHdG, total antioxidant capacity) in the cerebrospinal fluid (CSF) of healthy humans across a wide age range (24-91 years). CSF was collected from consenting patients who required a spinal tap for the administration of anesthetic. CSF of participants aged >45 years was found to contain increased levels of lipid peroxidation (F2-isoprostanes) (p = 0.04) and inflammation (IL-6) (p = 0.00) and decreased levels of both total antioxidant capacity (p = 0.00) and NAD(H) (p = 0.05), compared to their younger counterparts. A positive association was also observed between plasma [NAD(H)] and CSF NAD(H) levels (p = 0.03). Further analysis of the data identified a relationship between alcohol intake and CSF [NAD(H)] and markers of inflammation. The CSF of participants who consumed >1 standard drink of alcohol per day contained lower levels of NAD(H) compared to those who consumed no alcohol (p<0.05). An increase in CSF IL-6 was observed in participants who reported drinking >0-1 (p<0.05) and >1 (p<0.05) standard alcoholic drinks per day compared to those who did not drink alcohol. Taken together these data suggest a progressive age associated increase in oxidative damage, inflammation and reduced [NAD(H)] in the brain which may be exacerbated by alcohol intake.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0085335</identifier><identifier>PMID: 24454842</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>8-Hydroxydeoxyguanosine ; Adenine ; Adult ; Age ; Aged ; Aging ; Aging - cerebrospinal fluid ; Aging - metabolism ; Alcohol Drinking - cerebrospinal fluid ; Alcohol use ; Alcoholic beverages ; Antioxidants ; Antioxidants (Nutrients) ; Apoptosis ; Beverages ; Biology ; Biomarkers - cerebrospinal fluid ; Brain ; Brain damage ; Brain research ; Cerebrospinal fluid ; Chemical compounds ; Chemistry ; Cytokines ; Data processing ; Deoxyribonucleic acid ; DNA ; DNA repair ; Drinking behavior ; Epigenetic inheritance ; Hospitals ; Humans ; Inflammation ; Inflammation - cerebrospinal fluid ; Information processing ; Interleukin 6 ; Isoprostanes ; Life Style ; Lifestyles ; Lipid peroxidation ; Lipids ; Male ; Markers ; Medicine ; Metabolism ; Middle Aged ; NAD ; NAD - cerebrospinal fluid ; Nervous system ; Neurodegeneration ; Niacinamide ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Oxidative Stress ; Peroxidation ; Pharmacology ; Physiology ; Proteins ; Rodents ; Sex Characteristics ; Signaling ; Studies ; Tissues ; Young Adult</subject><ispartof>PloS one, 2014-01, Vol.9 (1), p.e85335-e85335</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Guest et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Guest et al 2014 Guest et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c644t-4e8a240286d16e16f0d984b3d8cb6de7e574e3b71190fa93e8704dd465ec20263</citedby><cites>FETCH-LOGICAL-c644t-4e8a240286d16e16f0d984b3d8cb6de7e574e3b71190fa93e8704dd465ec20263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891813/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891813/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27902,27903,53768,53770,79345,79346</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24454842$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Arendt, Thomas</contributor><creatorcontrib>Guest, Jade</creatorcontrib><creatorcontrib>Grant, Ross</creatorcontrib><creatorcontrib>Mori, Trevor A</creatorcontrib><creatorcontrib>Croft, Kevin D</creatorcontrib><title>Changes in oxidative damage, inflammation and [NAD(H)] with age in cerebrospinal fluid</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>An extensive body of evidence indicates that oxidative stress and inflammation play a central role in the degenerative changes of systemic tissues in aging. However a comparatively limited amount of data is available to verify whether these processes also contribute to normal aging within the brain. High levels of oxidative damage results in key cellular changes including a reduction in available nicotinamide adenine dinucleotide (NAD(+)), an essential molecule required for a number of vital cellular processes including DNA repair, immune signaling and epigenetic processing. In this study we quantified changes in [NAD(H)] and markers of inflammation and oxidative damage (F2-isoprostanes, 8-OHdG, total antioxidant capacity) in the cerebrospinal fluid (CSF) of healthy humans across a wide age range (24-91 years). CSF was collected from consenting patients who required a spinal tap for the administration of anesthetic. CSF of participants aged >45 years was found to contain increased levels of lipid peroxidation (F2-isoprostanes) (p = 0.04) and inflammation (IL-6) (p = 0.00) and decreased levels of both total antioxidant capacity (p = 0.00) and NAD(H) (p = 0.05), compared to their younger counterparts. A positive association was also observed between plasma [NAD(H)] and CSF NAD(H) levels (p = 0.03). Further analysis of the data identified a relationship between alcohol intake and CSF [NAD(H)] and markers of inflammation. The CSF of participants who consumed >1 standard drink of alcohol per day contained lower levels of NAD(H) compared to those who consumed no alcohol (p<0.05). An increase in CSF IL-6 was observed in participants who reported drinking >0-1 (p<0.05) and >1 (p<0.05) standard alcoholic drinks per day compared to those who did not drink alcohol. Taken together these data suggest a progressive age associated increase in oxidative damage, inflammation and reduced [NAD(H)] in the brain which may be exacerbated by alcohol intake.</description><subject>8-Hydroxydeoxyguanosine</subject><subject>Adenine</subject><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Aging</subject><subject>Aging - cerebrospinal fluid</subject><subject>Aging - metabolism</subject><subject>Alcohol Drinking - cerebrospinal fluid</subject><subject>Alcohol use</subject><subject>Alcoholic beverages</subject><subject>Antioxidants</subject><subject>Antioxidants (Nutrients)</subject><subject>Apoptosis</subject><subject>Beverages</subject><subject>Biology</subject><subject>Biomarkers - cerebrospinal fluid</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Brain research</subject><subject>Cerebrospinal fluid</subject><subject>Chemical compounds</subject><subject>Chemistry</subject><subject>Cytokines</subject><subject>Data processing</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA repair</subject><subject>Drinking behavior</subject><subject>Epigenetic inheritance</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - cerebrospinal fluid</subject><subject>Information processing</subject><subject>Interleukin 6</subject><subject>Isoprostanes</subject><subject>Life Style</subject><subject>Lifestyles</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Male</subject><subject>Markers</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>NAD</subject><subject>NAD - cerebrospinal fluid</subject><subject>Nervous system</subject><subject>Neurodegeneration</subject><subject>Niacinamide</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Oxidative Stress</subject><subject>Peroxidation</subject><subject>Pharmacology</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Sex Characteristics</subject><subject>Signaling</subject><subject>Studies</subject><subject>Tissues</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptUstu1DAUjRCIlsIfIIjEpkjM4FdsZ4M0GiitVMEG2CBkOfZNxqMkntpJgb_H6aRVB1Ve2Lo-59zXybKXGC0xFfj91o-h1-1y53tYIiQLSotH2TEuKVlwgujje--j7FmMW4QKKjl_mh0RxgomGTnOfqw3um8g5q7P_R9n9eCuIbe60w28S8G61V2Xgr7PdW_zn19WH0_P3_7Kf7thkyfMxDMQoAo-7lyqJ6_b0dnn2ZNatxFezPdJ9v3s07f1-eLy6-eL9epyYThjw4KB1IQhIrnFHDCvkS0lq6iVpuIWBBSCAa0ExiWqdUlBCsSsZbwAQxDh9CR7vdfdtT6qeSRRYSYEo1RQlhAXe4T1eqt2wXU6_FVeO3UT8KFROgzOtKAM1UVVY2JFzVmFoYQCl7VGzAgiSjxl-zBnG6sOrIF-CLo9ED386d1GNf5aUVliiWkSOJ0Fgr8aIQ6qc9FA2-oe_DjVXRJeUsRwgr75D_pwdzOq0amBtC6f8ppJVK2YkJIXhZQJtXwAlY6Fzpnkn9ql-AGB7QkmrTUGqO96xEhN7rstRk3uU7P7Eu3V_fnckW7tRv8BVmXVXw</recordid><startdate>20140114</startdate><enddate>20140114</enddate><creator>Guest, Jade</creator><creator>Grant, Ross</creator><creator>Mori, Trevor A</creator><creator>Croft, Kevin D</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140114</creationdate><title>Changes in oxidative damage, inflammation and [NAD(H)] with age in cerebrospinal fluid</title><author>Guest, Jade ; Grant, Ross ; Mori, Trevor A ; Croft, Kevin D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c644t-4e8a240286d16e16f0d984b3d8cb6de7e574e3b71190fa93e8704dd465ec20263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>8-Hydroxydeoxyguanosine</topic><topic>Adenine</topic><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Aging</topic><topic>Aging - cerebrospinal fluid</topic><topic>Aging - metabolism</topic><topic>Alcohol Drinking - cerebrospinal fluid</topic><topic>Alcohol use</topic><topic>Alcoholic beverages</topic><topic>Antioxidants</topic><topic>Antioxidants (Nutrients)</topic><topic>Apoptosis</topic><topic>Beverages</topic><topic>Biology</topic><topic>Biomarkers - cerebrospinal fluid</topic><topic>Brain</topic><topic>Brain damage</topic><topic>Brain research</topic><topic>Cerebrospinal fluid</topic><topic>Chemical compounds</topic><topic>Chemistry</topic><topic>Cytokines</topic><topic>Data processing</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA repair</topic><topic>Drinking behavior</topic><topic>Epigenetic inheritance</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - cerebrospinal fluid</topic><topic>Information processing</topic><topic>Interleukin 6</topic><topic>Isoprostanes</topic><topic>Life Style</topic><topic>Lifestyles</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Male</topic><topic>Markers</topic><topic>Medicine</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>NAD</topic><topic>NAD - cerebrospinal fluid</topic><topic>Nervous system</topic><topic>Neurodegeneration</topic><topic>Niacinamide</topic><topic>Nicotinamide</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Oxidative Stress</topic><topic>Peroxidation</topic><topic>Pharmacology</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Sex Characteristics</topic><topic>Signaling</topic><topic>Studies</topic><topic>Tissues</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guest, Jade</creatorcontrib><creatorcontrib>Grant, Ross</creatorcontrib><creatorcontrib>Mori, Trevor A</creatorcontrib><creatorcontrib>Croft, Kevin D</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guest, Jade</au><au>Grant, Ross</au><au>Mori, Trevor A</au><au>Croft, Kevin D</au><au>Arendt, Thomas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in oxidative damage, inflammation and [NAD(H)] with age in cerebrospinal fluid</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-01-14</date><risdate>2014</risdate><volume>9</volume><issue>1</issue><spage>e85335</spage><epage>e85335</epage><pages>e85335-e85335</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>An extensive body of evidence indicates that oxidative stress and inflammation play a central role in the degenerative changes of systemic tissues in aging. However a comparatively limited amount of data is available to verify whether these processes also contribute to normal aging within the brain. High levels of oxidative damage results in key cellular changes including a reduction in available nicotinamide adenine dinucleotide (NAD(+)), an essential molecule required for a number of vital cellular processes including DNA repair, immune signaling and epigenetic processing. In this study we quantified changes in [NAD(H)] and markers of inflammation and oxidative damage (F2-isoprostanes, 8-OHdG, total antioxidant capacity) in the cerebrospinal fluid (CSF) of healthy humans across a wide age range (24-91 years). CSF was collected from consenting patients who required a spinal tap for the administration of anesthetic. CSF of participants aged >45 years was found to contain increased levels of lipid peroxidation (F2-isoprostanes) (p = 0.04) and inflammation (IL-6) (p = 0.00) and decreased levels of both total antioxidant capacity (p = 0.00) and NAD(H) (p = 0.05), compared to their younger counterparts. A positive association was also observed between plasma [NAD(H)] and CSF NAD(H) levels (p = 0.03). Further analysis of the data identified a relationship between alcohol intake and CSF [NAD(H)] and markers of inflammation. The CSF of participants who consumed >1 standard drink of alcohol per day contained lower levels of NAD(H) compared to those who consumed no alcohol (p<0.05). An increase in CSF IL-6 was observed in participants who reported drinking >0-1 (p<0.05) and >1 (p<0.05) standard alcoholic drinks per day compared to those who did not drink alcohol. Taken together these data suggest a progressive age associated increase in oxidative damage, inflammation and reduced [NAD(H)] in the brain which may be exacerbated by alcohol intake.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24454842</pmid><doi>10.1371/journal.pone.0085335</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 8-Hydroxydeoxyguanosine Adenine Adult Age Aged Aging Aging - cerebrospinal fluid Aging - metabolism Alcohol Drinking - cerebrospinal fluid Alcohol use Alcoholic beverages Antioxidants Antioxidants (Nutrients) Apoptosis Beverages Biology Biomarkers - cerebrospinal fluid Brain Brain damage Brain research Cerebrospinal fluid Chemical compounds Chemistry Cytokines Data processing Deoxyribonucleic acid DNA DNA repair Drinking behavior Epigenetic inheritance Hospitals Humans Inflammation Inflammation - cerebrospinal fluid Information processing Interleukin 6 Isoprostanes Life Style Lifestyles Lipid peroxidation Lipids Male Markers Medicine Metabolism Middle Aged NAD NAD - cerebrospinal fluid Nervous system Neurodegeneration Niacinamide Nicotinamide Nicotinamide adenine dinucleotide Oxidative Stress Peroxidation Pharmacology Physiology Proteins Rodents Sex Characteristics Signaling Studies Tissues Young Adult |
| title | Changes in oxidative damage, inflammation and [NAD(H)] with age in cerebrospinal fluid |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T09%3A15%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Changes%20in%20oxidative%20damage,%20inflammation%20and%20%5BNAD(H)%5D%20with%20age%20in%20cerebrospinal%20fluid&rft.jtitle=PloS%20one&rft.au=Guest,%20Jade&rft.date=2014-01-14&rft.volume=9&rft.issue=1&rft.spage=e85335&rft.epage=e85335&rft.pages=e85335-e85335&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0085335&rft_dat=%3Cgale_plos_%3EA478865588%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1477433734&rft_id=info:pmid/24454842&rft_galeid=A478865588&rft_doaj_id=oai_doaj_org_article_c3a5bf12d7f64b1e9e519fa04c727916&rfr_iscdi=true |