8OHdG levels in brain do not indicate oxidative DNA damage in Alzheimer's disease
Accumulation of oxidative DNA damage has been proposed to underlie aging and neurodegenerative diseases such as Alzheimer's Disease (AD). The DNA adduct 8-hydroxy-2′-deoxyguanosine (8OHdG) is considered a good indicator of oxidative DNA damage. To investigate whether this type of DNA damage is...
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| Veröffentlicht in: | Neurobiology of aging 1996-11, Vol.17 (6), p.819-826 |
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| container_title | Neurobiology of aging |
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| creator | Te Koppele, J.M. Lucassen, P.J. Sakkee, A.N. Van Asten, J.G. Ravid, R. Swaab, D.F. Van Bezooijen, C.F.A. |
| description | Accumulation of oxidative DNA damage has been proposed to underlie aging and neurodegenerative diseases such as Alzheimer's Disease (AD). The DNA adduct 8-hydroxy-2′-deoxyguanosine (8OHdG) is considered a good indicator of oxidative DNA damage. To investigate whether this type of DNA damage is involved in AD etiology, 8OHdG levels were determined in postmortem human brain tissue of controls and AD patients (in frontal, occipital, and temporal cortex and in hippocampal tissue). Parametric studies in rat revealed no influences of postmortem delay, repeated freezing/thawing or storage time. In human brain, approximately two 8OHdG molecules were present per 10
5 2′-deoxyguanosines. In AD patients and controls, 8OHdG-levels were not related to age, sex, or brain region. Also, no differences were found between controls and AD patients. It was concluded that 8OHdG in nuclear DNA, although present throughout the brain in fairly high amounts, does not accumulate with age, nor does it appear to be involved in AD. More detailed studies are required to extend this conclusion to other types of oxidative damage. |
| doi_str_mv | 10.1016/S0197-4580(96)00165-0 |
| format | Article |
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5 2′-deoxyguanosines. In AD patients and controls, 8OHdG-levels were not related to age, sex, or brain region. Also, no differences were found between controls and AD patients. It was concluded that 8OHdG in nuclear DNA, although present throughout the brain in fairly high amounts, does not accumulate with age, nor does it appear to be involved in AD. More detailed studies are required to extend this conclusion to other types of oxidative damage.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/S0197-4580(96)00165-0</identifier><identifier>PMID: 9363791</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>8-Hydroxy-2′-deoxyguanosine ; Adult ; Aged ; Aging ; Alzheimer Disease - metabolism ; Alzheimer's Disease ; Biological and medical sciences ; Brain Chemistry - physiology ; Cerebral Cortex - chemistry ; Chromatography, High Pressure Liquid ; Cortex ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - metabolism ; DNA - analysis ; DNA damage ; DNA Damage - physiology ; Electrochemistry ; Female ; Hippocampus ; Hippocampus - chemistry ; HPLC-ECD ; Human brain ; Humans ; Hydrolysis ; Male ; Medical sciences ; Middle Aged ; Neurology ; Oxidative Stress - physiology ; Oxygen radicals ; Postmortem Changes ; Specimen Handling</subject><ispartof>Neurobiology of aging, 1996-11, Vol.17 (6), p.819-826</ispartof><rights>1996</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3820-9efd4e241c1294e51028ff215fa040aae90332214c80942076e721aef17dede3</citedby><cites>FETCH-LOGICAL-c3820-9efd4e241c1294e51028ff215fa040aae90332214c80942076e721aef17dede3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0197-4580(96)00165-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2516273$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9363791$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Te Koppele, J.M.</creatorcontrib><creatorcontrib>Lucassen, P.J.</creatorcontrib><creatorcontrib>Sakkee, A.N.</creatorcontrib><creatorcontrib>Van Asten, J.G.</creatorcontrib><creatorcontrib>Ravid, R.</creatorcontrib><creatorcontrib>Swaab, D.F.</creatorcontrib><creatorcontrib>Van Bezooijen, C.F.A.</creatorcontrib><title>8OHdG levels in brain do not indicate oxidative DNA damage in Alzheimer's disease</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Accumulation of oxidative DNA damage has been proposed to underlie aging and neurodegenerative diseases such as Alzheimer's Disease (AD). The DNA adduct 8-hydroxy-2′-deoxyguanosine (8OHdG) is considered a good indicator of oxidative DNA damage. To investigate whether this type of DNA damage is involved in AD etiology, 8OHdG levels were determined in postmortem human brain tissue of controls and AD patients (in frontal, occipital, and temporal cortex and in hippocampal tissue). Parametric studies in rat revealed no influences of postmortem delay, repeated freezing/thawing or storage time. In human brain, approximately two 8OHdG molecules were present per 10
5 2′-deoxyguanosines. In AD patients and controls, 8OHdG-levels were not related to age, sex, or brain region. Also, no differences were found between controls and AD patients. It was concluded that 8OHdG in nuclear DNA, although present throughout the brain in fairly high amounts, does not accumulate with age, nor does it appear to be involved in AD. More detailed studies are required to extend this conclusion to other types of oxidative damage.</description><subject>8-Hydroxy-2′-deoxyguanosine</subject><subject>Adult</subject><subject>Aged</subject><subject>Aging</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's Disease</subject><subject>Biological and medical sciences</subject><subject>Brain Chemistry - physiology</subject><subject>Cerebral Cortex - chemistry</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Cortex</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - metabolism</subject><subject>DNA - analysis</subject><subject>DNA damage</subject><subject>DNA Damage - physiology</subject><subject>Electrochemistry</subject><subject>Female</subject><subject>Hippocampus</subject><subject>Hippocampus - chemistry</subject><subject>HPLC-ECD</subject><subject>Human brain</subject><subject>Humans</subject><subject>Hydrolysis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Oxidative Stress - physiology</subject><subject>Oxygen radicals</subject><subject>Postmortem Changes</subject><subject>Specimen Handling</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtPHDEMgKOqiC60PwFpDqjAYaidSSaTE1rxllBRVe5RSDxtqnlAMrsCfn2z7GqvXBw5_mxHXxg7QDhFwPrHb0CtSiEbONb1CeQrWcInNkMpmxKFVp_ZbIt8YXsp_QMAJVS9y3Z1VVdK44z9au5v_HXR0ZK6VISheIw2Rz8Wwzjl3AdnJyrGl-DtFJZUXPycF9729g-t6Hn39pdCT_EoFT4ksom-sp3Wdom-bc599nB1-XB-U97dX9-ez-9KVzUcSk2tF8QFOuRakETgTdtylK0FAdaShqriHIVrQAsOqibF0VKLypOnap99X499iuPzgtJk-pAcdZ0daFwkoxqVRQj9IYhSy2wFMijXoItjSpFa8xRDb-OrQTAr5eZduVn5NLo278rNqu9gs2Dx2JPfdm0c5_rhpm6Ts10b7eBC2mJcYs1VlbGzNZY_gpaBokku0ODIh0huMn4MHzzkP3Wemts</recordid><startdate>199611</startdate><enddate>199611</enddate><creator>Te Koppele, J.M.</creator><creator>Lucassen, P.J.</creator><creator>Sakkee, A.N.</creator><creator>Van Asten, J.G.</creator><creator>Ravid, R.</creator><creator>Swaab, D.F.</creator><creator>Van Bezooijen, C.F.A.</creator><general>Elsevier Inc</general><general>Elsevier Science</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>199611</creationdate><title>8OHdG levels in brain do not indicate oxidative DNA damage in Alzheimer's disease</title><author>Te Koppele, J.M. ; Lucassen, P.J. ; Sakkee, A.N. ; Van Asten, J.G. ; Ravid, R. ; Swaab, D.F. ; Van Bezooijen, C.F.A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3820-9efd4e241c1294e51028ff215fa040aae90332214c80942076e721aef17dede3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>8-Hydroxy-2′-deoxyguanosine</topic><topic>Adult</topic><topic>Aged</topic><topic>Aging</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's Disease</topic><topic>Biological and medical sciences</topic><topic>Brain Chemistry - physiology</topic><topic>Cerebral Cortex - chemistry</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Cortex</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - metabolism</topic><topic>DNA - analysis</topic><topic>DNA damage</topic><topic>DNA Damage - physiology</topic><topic>Electrochemistry</topic><topic>Female</topic><topic>Hippocampus</topic><topic>Hippocampus - chemistry</topic><topic>HPLC-ECD</topic><topic>Human brain</topic><topic>Humans</topic><topic>Hydrolysis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Oxidative Stress - physiology</topic><topic>Oxygen radicals</topic><topic>Postmortem Changes</topic><topic>Specimen Handling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Te Koppele, J.M.</creatorcontrib><creatorcontrib>Lucassen, P.J.</creatorcontrib><creatorcontrib>Sakkee, A.N.</creatorcontrib><creatorcontrib>Van Asten, J.G.</creatorcontrib><creatorcontrib>Ravid, R.</creatorcontrib><creatorcontrib>Swaab, D.F.</creatorcontrib><creatorcontrib>Van Bezooijen, C.F.A.</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Te Koppele, J.M.</au><au>Lucassen, P.J.</au><au>Sakkee, A.N.</au><au>Van Asten, J.G.</au><au>Ravid, R.</au><au>Swaab, D.F.</au><au>Van Bezooijen, C.F.A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>8OHdG levels in brain do not indicate oxidative DNA damage in Alzheimer's disease</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>1996-11</date><risdate>1996</risdate><volume>17</volume><issue>6</issue><spage>819</spage><epage>826</epage><pages>819-826</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>Accumulation of oxidative DNA damage has been proposed to underlie aging and neurodegenerative diseases such as Alzheimer's Disease (AD). The DNA adduct 8-hydroxy-2′-deoxyguanosine (8OHdG) is considered a good indicator of oxidative DNA damage. To investigate whether this type of DNA damage is involved in AD etiology, 8OHdG levels were determined in postmortem human brain tissue of controls and AD patients (in frontal, occipital, and temporal cortex and in hippocampal tissue). Parametric studies in rat revealed no influences of postmortem delay, repeated freezing/thawing or storage time. In human brain, approximately two 8OHdG molecules were present per 10
5 2′-deoxyguanosines. In AD patients and controls, 8OHdG-levels were not related to age, sex, or brain region. Also, no differences were found between controls and AD patients. It was concluded that 8OHdG in nuclear DNA, although present throughout the brain in fairly high amounts, does not accumulate with age, nor does it appear to be involved in AD. More detailed studies are required to extend this conclusion to other types of oxidative damage.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>9363791</pmid><doi>10.1016/S0197-4580(96)00165-0</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 8-Hydroxy-2′-deoxyguanosine Adult Aged Aging Alzheimer Disease - metabolism Alzheimer's Disease Biological and medical sciences Brain Chemistry - physiology Cerebral Cortex - chemistry Chromatography, High Pressure Liquid Cortex Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Deoxyguanosine - analogs & derivatives Deoxyguanosine - metabolism DNA - analysis DNA damage DNA Damage - physiology Electrochemistry Female Hippocampus Hippocampus - chemistry HPLC-ECD Human brain Humans Hydrolysis Male Medical sciences Middle Aged Neurology Oxidative Stress - physiology Oxygen radicals Postmortem Changes Specimen Handling |
| title | 8OHdG levels in brain do not indicate oxidative DNA damage in Alzheimer's disease |
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