Normal Mitochondrial Genome in Brain from Patients with Parkinson's Disease and Complex I Defect
: The mitochondrial genome codes for 13 proteins which are located in the respiratory chain. In postmortem brain of patients with Parkinson's disease, decreased activity of complex I of the respiratory chain could be demonstrated. Because seven subunits of complex I are coded by the mitochondri...
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| Veröffentlicht in: | Journal of neurochemistry 1990-11, Vol.55 (5), p.1810-1812 |
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| container_issue | 5 |
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| container_title | Journal of neurochemistry |
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| creator | Lestienne, P. Nelson, J. Riederer, P. Jellinger, K. Reichmann, H. |
| description | : The mitochondrial genome codes for 13 proteins which are located in the respiratory chain. In postmortem brain of patients with Parkinson's disease, decreased activity of complex I of the respiratory chain could be demonstrated. Because seven subunits of complex I are coded by the mitochondrial genome, we analyzed the mitochondrial DNA of human postmortem substantia nigra, putamen, and frontal cortex by the Southern blot technique. No deletions of the mitochondrial genome could be demonstrated, thus indicating that either subunits which are encoded by the nuclear genome are decreased or enzyme activity is diminished by metabolites, toxins, or increase of Fe3+. |
| doi_str_mv | 10.1111/j.1471-4159.1990.tb04973.x |
| format | Article |
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In postmortem brain of patients with Parkinson's disease, decreased activity of complex I of the respiratory chain could be demonstrated. Because seven subunits of complex I are coded by the mitochondrial genome, we analyzed the mitochondrial DNA of human postmortem substantia nigra, putamen, and frontal cortex by the Southern blot technique. No deletions of the mitochondrial genome could be demonstrated, thus indicating that either subunits which are encoded by the nuclear genome are decreased or enzyme activity is diminished by metabolites, toxins, or increase of Fe3+.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.1990.tb04973.x</identifier><identifier>PMID: 2120389</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; Biological and medical sciences ; Brain - metabolism ; Brain - physiopathology ; Complex I defect ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA - metabolism ; Female ; Genomic Library ; Humans ; Male ; Medical sciences ; Middle Aged ; Mitochondria - physiology ; Mitochondrial genome ; NAD(P)H Dehydrogenase (Quinone) ; Neurology ; Parkinson Disease - genetics ; Parkinson Disease - metabolism ; Parkinson's disease ; Quinone Reductases - metabolism ; Respiratory chain</subject><ispartof>Journal of neurochemistry, 1990-11, Vol.55 (5), p.1810-1812</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3990-987419b87c07647f710bc8e546b2002f30ea44dbda4b5f66f004595ea2b140193</citedby><cites>FETCH-LOGICAL-c3990-987419b87c07647f710bc8e546b2002f30ea44dbda4b5f66f004595ea2b140193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.1990.tb04973.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.1990.tb04973.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5596522$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2120389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lestienne, P.</creatorcontrib><creatorcontrib>Nelson, J.</creatorcontrib><creatorcontrib>Riederer, P.</creatorcontrib><creatorcontrib>Jellinger, K.</creatorcontrib><creatorcontrib>Reichmann, H.</creatorcontrib><title>Normal Mitochondrial Genome in Brain from Patients with Parkinson's Disease and Complex I Defect</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: The mitochondrial genome codes for 13 proteins which are located in the respiratory chain. In postmortem brain of patients with Parkinson's disease, decreased activity of complex I of the respiratory chain could be demonstrated. Because seven subunits of complex I are coded by the mitochondrial genome, we analyzed the mitochondrial DNA of human postmortem substantia nigra, putamen, and frontal cortex by the Southern blot technique. No deletions of the mitochondrial genome could be demonstrated, thus indicating that either subunits which are encoded by the nuclear genome are decreased or enzyme activity is diminished by metabolites, toxins, or increase of Fe3+.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>Complex I defect</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA - metabolism</subject><subject>Female</subject><subject>Genomic Library</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mitochondria - physiology</subject><subject>Mitochondrial genome</subject><subject>NAD(P)H Dehydrogenase (Quinone)</subject><subject>Neurology</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson's disease</subject><subject>Quinone Reductases - metabolism</subject><subject>Respiratory chain</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkEtv3CAUhVHVKpkm_QmRUFS1KzuA8YNuonTS5qE8umjXFOOLwsSGCXiUyb8v1liz711wdXXOAe6H0CklOU11tsopr2nGaSlyKgTJx5ZwURf59h1a7KX3aEEIY1lBODtEH2NcEUIrXtEDdMAoI0UjFujvgw-D6vG9Hb1-8q4LNk1X4PwA2Dr8Pah0muAH_EuNFtwY8asdn9IUnq2L3n2N-NJGUBGwch1e-mHdwxbf4EswoMdj9MGoPsKnuR-hPz9__F5eZ3ePVzfLi7tMF2mDTDQ1p6Jtak3qitempqTVDZS8alnawhQEFOdd2ynelqaqDCG8FCUo1lJOqCiO0JfdvevgXzYQRznYqKHvlQO_ibJJAVZUk_HbzqiDjzGAketgBxXeJCVywitXcmIoJ4ZywitnvHKbwifzK5t2gG4fnXkm_fOsq6hVb4Jy2sa9rSxFVTKWbOc726vt4e0_PiBvH5a0oaT4B5TslhA</recordid><startdate>199011</startdate><enddate>199011</enddate><creator>Lestienne, P.</creator><creator>Nelson, J.</creator><creator>Riederer, P.</creator><creator>Jellinger, K.</creator><creator>Reichmann, H.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</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>7X8</scope></search><sort><creationdate>199011</creationdate><title>Normal Mitochondrial Genome in Brain from Patients with Parkinson's Disease and Complex I Defect</title><author>Lestienne, P. ; Nelson, J. ; Riederer, P. ; Jellinger, K. ; Reichmann, H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3990-987419b87c07647f710bc8e546b2002f30ea44dbda4b5f66f004595ea2b140193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain - physiopathology</topic><topic>Complex I defect</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>DNA - metabolism</topic><topic>Female</topic><topic>Genomic Library</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mitochondria - physiology</topic><topic>Mitochondrial genome</topic><topic>NAD(P)H Dehydrogenase (Quinone)</topic><topic>Neurology</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson's disease</topic><topic>Quinone Reductases - metabolism</topic><topic>Respiratory chain</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lestienne, P.</creatorcontrib><creatorcontrib>Nelson, J.</creatorcontrib><creatorcontrib>Riederer, P.</creatorcontrib><creatorcontrib>Jellinger, K.</creatorcontrib><creatorcontrib>Reichmann, H.</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>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lestienne, P.</au><au>Nelson, J.</au><au>Riederer, P.</au><au>Jellinger, K.</au><au>Reichmann, H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Normal Mitochondrial Genome in Brain from Patients with Parkinson's Disease and Complex I Defect</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>1990-11</date><risdate>1990</risdate><volume>55</volume><issue>5</issue><spage>1810</spage><epage>1812</epage><pages>1810-1812</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: The mitochondrial genome codes for 13 proteins which are located in the respiratory chain. In postmortem brain of patients with Parkinson's disease, decreased activity of complex I of the respiratory chain could be demonstrated. Because seven subunits of complex I are coded by the mitochondrial genome, we analyzed the mitochondrial DNA of human postmortem substantia nigra, putamen, and frontal cortex by the Southern blot technique. No deletions of the mitochondrial genome could be demonstrated, thus indicating that either subunits which are encoded by the nuclear genome are decreased or enzyme activity is diminished by metabolites, toxins, or increase of Fe3+.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>2120389</pmid><doi>10.1111/j.1471-4159.1990.tb04973.x</doi><tpages>3</tpages></addata></record> |
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| ispartof | Journal of neurochemistry, 1990-11, Vol.55 (5), p.1810-1812 |
| issn | 0022-3042 1471-4159 |
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| subjects | Aged Biological and medical sciences Brain - metabolism Brain - physiopathology Complex I defect Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA - metabolism Female Genomic Library Humans Male Medical sciences Middle Aged Mitochondria - physiology Mitochondrial genome NAD(P)H Dehydrogenase (Quinone) Neurology Parkinson Disease - genetics Parkinson Disease - metabolism Parkinson's disease Quinone Reductases - metabolism Respiratory chain |
| title | Normal Mitochondrial Genome in Brain from Patients with Parkinson's Disease and Complex I Defect |
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