Multinuclear Magnetic Resonance Spectroscopy for in Vivo Assessment of Mitochondrial Dysfunction in Parkinson's Disease
Identifieur interne : 000D42 ( Main/Exploration ); précédent : 000D41; suivant : 000D43Multinuclear Magnetic Resonance Spectroscopy for in Vivo Assessment of Mitochondrial Dysfunction in Parkinson's Disease
Auteurs : Claire Henchcliffe [États-Unis] ; Dikoma C. Shungu [États-Unis] ; Xiangling Mao [États-Unis] ; Chaorui Huang [États-Unis] ; Melissa J. Nirenberg [États-Unis] ; Bruce G. Jenkins [États-Unis] ; M. Flint Beal [États-Unis]Source :
- Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders [ 0077-8923 ] ; 2008-12.
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Abstract
Parkinson's disease (PD) is a common and often devastating neurodegenerative disease affecting up to one million individuals in the United States alone. Multiple lines of evidence support mitochondrial dysfunction as a primary or secondary event in PD pathogenesis; a better understanding, therefore, of how mitochondrial function is altered in vivo in brain tissue in PD is a critical step toward developing potential PD biomarkers. In vivo study of mitochondrial metabolism in human subjects has previously been technically challenging. However, proton and phosphorus magnetic resonance spectroscopy (1H and 31P MRS) are powerful noninvasive techniques that allow evaluation in vivo of lactate, a marker of anaerobic glycolysis, and high energy phosphates, such as adenosine triphosphate and phosphocreatine, directly reflecting mitochondrial function. This article reviews previous 1H and 31P MRS studies in PD, which demonstrate metabolic abnormalities consistent with mitochondrial dysfunction, and then presents recent 1H MRS data revealing abnormally elevated lactate levels in PD subjects.
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DOI: 10.1196/annals.1427.037
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Flint Beal</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2008-12">2008-12</date><biblScope unit="volume">1147</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="206">206</biblScope><biblScope unit="page" to="220">220</biblScope></imprint><idno type="ISSN">0077-8923</idno></series><idno type="istex">604B862686EF18795E630BA215678FE01B1F0C09</idno><idno type="DOI">10.1196/annals.1427.037</idno><idno type="ArticleID">NYAS1147037</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>high‐energy phosphates</term><term>lactate</term><term>magnetic resonance spectroscopy</term><term>mitochondria</term><term>neurodegenerative disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a common and often devastating neurodegenerative disease affecting up to one million individuals in the United States alone. Multiple lines of evidence support mitochondrial dysfunction as a primary or secondary event in PD pathogenesis; a better understanding, therefore, of how mitochondrial function is altered in vivo in brain tissue in PD is a critical step toward developing potential PD biomarkers. In vivo study of mitochondrial metabolism in human subjects has previously been technically challenging. However, proton and phosphorus magnetic resonance spectroscopy (1H and 31P MRS) are powerful noninvasive techniques that allow evaluation in vivo of lactate, a marker of anaerobic glycolysis, and high energy phosphates, such as adenosine triphosphate and phosphocreatine, directly reflecting mitochondrial function. This article reviews previous 1H and 31P MRS studies in PD, which demonstrate metabolic abnormalities consistent with mitochondrial dysfunction, and then presents recent 1H MRS data revealing abnormally elevated lactate levels in PD subjects.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Henchcliffe, Claire" sort="Henchcliffe, Claire" uniqKey="Henchcliffe C" first="Claire" last="Henchcliffe">Claire Henchcliffe</name></region><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><name sortKey="Huang, Chaorui" sort="Huang, Chaorui" uniqKey="Huang C" first="Chaorui" last="Huang">Chaorui Huang</name><name sortKey="Jenkins, Bruce G" sort="Jenkins, Bruce G" uniqKey="Jenkins B" first="Bruce G." last="Jenkins">Bruce G. Jenkins</name><name sortKey="Mao, Xiangling" sort="Mao, Xiangling" uniqKey="Mao X" first="Xiangling" last="Mao">Xiangling Mao</name><name sortKey="Nirenberg, Melissa J" sort="Nirenberg, Melissa J" uniqKey="Nirenberg M" first="Melissa J." last="Nirenberg">Melissa J. Nirenberg</name><name sortKey="Shungu, Dikoma C" sort="Shungu, Dikoma C" uniqKey="Shungu D" first="Dikoma C." last="Shungu">Dikoma C. Shungu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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