Effect of aging and dopaminomimetic therapy on mitochondrial respiratory function in Parkinson's disease
Identifieur interne : 003322 ( Istex/Corpus ); précédent : 003321; suivant : 003323Effect of aging and dopaminomimetic therapy on mitochondrial respiratory function in Parkinson's disease
Auteurs : Daniele Bravi ; Jeffrey J. Anderson ; Fiorenzo Dagani ; Thomas L. Davis ; Rosaria Ferrari ; Marge Gillespie ; ChaseSource :
- Movement Disorders [ 0885-3185 ] ; 1992.
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Abstract
Oxygen consumption and enzyme activity were evaluted in platelet mitochondria from 17 patients with Parkinson's disease. In comparison with age‐matched controls, no consistent abnormality could be discerned in complex I, complex II‐III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.
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DOI: 10.1002/mds.870070307
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In comparison with age‐matched controls, no consistent abnormality could be discerned in complex I, complex II‐III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Daniele Bravi</name><affiliations><json:string>Experimental Therapeutics Branch, NINDS, NIH, Bethesda, Maryland, U.S.A.</json:string></affiliations></json:item><json:item><name>Jeffrey J. Anderson</name><affiliations><json:string>Experimental Therapeutics Branch, NINDS, NIH, Bethesda, Maryland, U.S.A.</json:string></affiliations></json:item><json:item><name>Fiorenzo Dagani</name><affiliations><json:string>Instiute of Pharmacology, University of Pavia, Pavia, Italy</json:string></affiliations></json:item><json:item><name>Thomas L. 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In comparison with age‐matched controls, no consistent abnormality could be discerned in complex I, complex II‐III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>Respiration</topic><topic>Lactate</topic><topic>Glucose</topic><topic>Platelets</topic><topic>Mitochondria</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>228</start><end>231</end><total>4</total></extent></part></relatedItem><identifier type="istex">CC5EF4266868D9B9A52A82A774207936C3DFFF8A</identifier><identifier type="DOI">10.1002/mds.870070307</identifier><identifier type="ArticleID">MDS870070307</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1992 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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