Assessment of brain iron and neuronal integrity in patients with Parkinson's disease using novel MRI contrasts
Identifieur interne : 001689 ( Main/Corpus ); précédent : 001688; suivant : 001690Assessment of brain iron and neuronal integrity in patients with Parkinson's disease using novel MRI contrasts
Auteurs : Shalom Michaeli ; Gülin Öz ; Dennis J. Sorce ; Michael Garwood ; Kamil Ugurbil ; Stacy Majestic ; Paul TuiteSource :
- Movement Disorders [ 0885-3185 ] ; 2007-02-15.
English descriptors
Abstract
Postmortem demonstration of increased iron in the substantia nigra (SN) is a well‐appreciated finding in Parkinson's disease (PD). Iron facilitates generation of free radicals, which are thought to play a role in dopamine neuronal loss. To date, however, magnetic resonance imaging (MRI) has failed to show significant in vivo differences in SN iron levels in subjects with PD versus control subjects. This finding may be due to the limitations in tissue contrasts achievable with conventional T1‐ and T2‐weighted MRI sequences that have been used. With the recent development of novel rotating frame transverse (T2ρ) and longitudinal (T1ρ) relaxation MRI methods that appear to be sensitive to iron and neuronal loss, respectively, we embarked on a study of 8 individuals with PD (Hoehn & Yahr, Stage II) and 8 age‐matched control subjects. Using these techniques with a 4T MRI magnet, we assessed iron deposits and neuronal integrity in the SN. First, T2ρ MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T2 MRI did not. Second, T1ρ measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. We show here that sub‐millimeter resolution T1ρ and T2ρ MRI relaxation methods can provide a noninvasive measure of iron content as well as evidence of neuronal loss in the midbrain of patients with PD. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21227
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Iron facilitates generation of free radicals, which are thought to play a role in dopamine neuronal loss. To date, however, magnetic resonance imaging (MRI) has failed to show significant in vivo differences in SN iron levels in subjects with PD versus control subjects. This finding may be due to the limitations in tissue contrasts achievable with conventional T1‐ and T2‐weighted MRI sequences that have been used. With the recent development of novel rotating frame transverse (T2ρ) and longitudinal (T1ρ) relaxation MRI methods that appear to be sensitive to iron and neuronal loss, respectively, we embarked on a study of 8 individuals with PD (Hoehn & Yahr, Stage II) and 8 age‐matched control subjects. Using these techniques with a 4T MRI magnet, we assessed iron deposits and neuronal integrity in the SN. First, T2ρ MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T2 MRI did not. Second, T1ρ measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. We show here that sub‐millimeter resolution T1ρ and T2ρ MRI relaxation methods can provide a noninvasive measure of iron content as well as evidence of neuronal loss in the midbrain of patients with PD. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Shalom Michaeli PhD</name><affiliations><json:string>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Gülin öz PhD</name><affiliations><json:string>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</json:string></affiliations></json:item><json:item><name>Dennis J. 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First, T2ρ MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T2 MRI did not. Second, T1ρ measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. 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Iron facilitates generation of free radicals, which are thought to play a role in dopamine neuronal loss. To date, however, magnetic resonance imaging (MRI) has failed to show significant in vivo differences in SN iron levels in subjects with PD versus control subjects. This finding may be due to the limitations in tissue contrasts achievable with conventional T1‐ and T2‐weighted MRI sequences that have been used. With the recent development of novel rotating frame transverse (T2ρ) and longitudinal (T1ρ) relaxation MRI methods that appear to be sensitive to iron and neuronal loss, respectively, we embarked on a study of 8 individuals with PD (Hoehn & Yahr, Stage II) and 8 age‐matched control subjects. Using these techniques with a 4T MRI magnet, we assessed iron deposits and neuronal integrity in the SN. First, T2ρ MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T2 MRI did not. Second, T1ρ measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. 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loss</keyword></keywordGroup><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>CA92004</fundingNumber><fundingNumber>RR08079</fundingNumber><fundingNumber>NS 40801</fundingNumber><fundingNumber>EB 00422</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Keck Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>MIND Institute</fundingAgency></fundingInfo><fundingInfo><fundingAgency>University of Minnesota Academic Health Center</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Minnesota Medical Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Postmortem demonstration of increased iron in the substantia nigra (SN) is a well‐appreciated finding in Parkinson's disease (PD). Iron facilitates generation of free radicals, which are thought to play a role in dopamine neuronal loss. To date, however, magnetic resonance imaging (MRI) has failed to show significant in vivo differences in SN iron levels in subjects with PD versus control subjects. This finding may be due to the limitations in tissue contrasts achievable with conventional T<sub>1</sub>‐ and T<sub>2</sub>‐weighted MRI sequences that have been used. With the recent development of novel rotating frame transverse (T<sub>2ρ</sub>) and longitudinal (T<sub>1ρ</sub>) relaxation MRI methods that appear to be sensitive to iron and neuronal loss, respectively, we embarked on a study of 8 individuals with PD (Hoehn & Yahr, Stage II) and 8 age‐matched control subjects. Using these techniques with a 4T MRI magnet, we assessed iron deposits and neuronal integrity in the SN. First, T<sub>2ρ</sub> MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T<sub>2</sub> MRI did not. Second, T<sub>1ρ</sub> measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. We show here that sub‐millimeter resolution T<sub>1ρ</sub> and T<sub>2ρ</sub> MRI relaxation methods can provide a <i>noninvasive measure</i> of iron content as well as evidence of neuronal loss in the midbrain of patients with PD. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Assessment of brain iron and neuronal integrity in patients with Parkinson's disease using novel MRI contrasts</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brain Iron in PD By T1ρ and T2ρ MRI</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Assessment of brain iron and neuronal integrity in patients with Parkinson's disease using novel MRI contrasts</title></titleInfo><name type="personal"><namePart type="given">Shalom</namePart><namePart type="family">Michaeli</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</affiliation><description>Correspondence: Center for Magnetic Resonance Research, Department of Radiology, University of Minnesota Medical School, 2021 6th Street SE, Minneapolis, MN 55455</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gülin</namePart><namePart type="family">öz</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dennis J.</namePart><namePart type="family">Sorce</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Garwood</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kamil</namePart><namePart type="family">Ugurbil</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Center for Magnetic Resonance Research and Department of Radiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stacy</namePart><namePart type="family">Majestic</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University of Minnesota, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul</namePart><namePart type="family">Tuite</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Minnesota, Minneapolis, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-02-15</dateIssued><dateCaptured encoding="w3cdtf">2006-06-02</dateCaptured><dateValid encoding="w3cdtf">2006-08-09</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">1</extent><extent unit="references">40</extent><extent unit="words">5442</extent></physicalDescription><abstract lang="en">Postmortem demonstration of increased iron in the substantia nigra (SN) is a well‐appreciated finding in Parkinson's disease (PD). Iron facilitates generation of free radicals, which are thought to play a role in dopamine neuronal loss. To date, however, magnetic resonance imaging (MRI) has failed to show significant in vivo differences in SN iron levels in subjects with PD versus control subjects. This finding may be due to the limitations in tissue contrasts achievable with conventional T1‐ and T2‐weighted MRI sequences that have been used. With the recent development of novel rotating frame transverse (T2ρ) and longitudinal (T1ρ) relaxation MRI methods that appear to be sensitive to iron and neuronal loss, respectively, we embarked on a study of 8 individuals with PD (Hoehn & Yahr, Stage II) and 8 age‐matched control subjects. Using these techniques with a 4T MRI magnet, we assessed iron deposits and neuronal integrity in the SN. First, T2ρ MRI, which is reflective of iron‐related dynamic dephasing mechanisms (e.g., chemical exchange and diffusion in the locally different magnetic susceptibilities), demonstrated a statistically significant difference between the PD and control group, while routine T2 MRI did not. Second, T1ρ measurements, which appear to reflect upon neuronal count, indicated neuronal loss in the SN in PD. We show here that sub‐millimeter resolution T1ρ and T2ρ MRI relaxation methods can provide a noninvasive measure of iron content as well as evidence of neuronal loss in the midbrain of patients with PD. © 2006 Movement Disorder Society</abstract><note type="funding">NIH - No. CA92004; No. RR08079; No. NS 40801; No. EB 00422; </note><note type="funding">Keck Foundation</note><note type="funding">MIND Institute</note><note type="funding">University of Minnesota Academic Health Center</note><note type="funding">Minnesota Medical Foundation</note><subject lang="en"><genre>Keywords</genre><topic>T1ρ and T2ρ MRI</topic><topic>iron load and distribution</topic><topic>neuronal loss</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><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research 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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>334</start><end>340</end><total>7</total></extent></part></relatedItem><identifier type="istex">6F1A503DEEFA2E3F2DE2C9151950119FB5ADF403</identifier><identifier type="DOI">10.1002/mds.21227</identifier><identifier type="ArticleID">MDS21227</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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