MovDisordV3, PascalFrancis, Corpus, bibRecord, 000219

Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy

Identifieur interne : 000219 ( PascalFrancis/Corpus ); précédent : 000218; suivant : 000220

Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy

Auteurs : Kai Boelmans ; Brigitte Holst ; Marc Hackius ; Jürgen Finsterbusch ; Christian Gerloff ; Jens Fiehler ; Alexander Münchau

Source :

Movement disorders [ 0885-3185 ] ; 2012.

RBID : Pascal:12-0198680

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Encéphale, Fer, Ophtalmoplégie supranucléaire, Noyau gris central, Imagerie RMN.

English descriptors

KwdEn :
- Basal ganglion, Encephalon, Iron, Nervous system diseases, Nuclear magnetic resonance imaging, Parkinson disease, Supranuclear ophthalmoplegia.

Abstract

It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2^*-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2^*-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.
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C07	`06`	`X`	`FRE`	`@0 Syndrome oculomoteur @5 43`
C07	`06`	`X`	`ENG`	`@0 Oculomotor syndrome @5 43`
C07	`06`	`X`	`SPA`	`@0 Oculomotricidad síndrome @5 43`
C07	`07`	`X`	`FRE`	`@0 Pathologie de l'oeil @5 44`
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Format Inist (serveur)

NO :	PASCAL 12-0198680 INIST
ET :	Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy
AU :	BOELMANS (Kai); HOLST (Brigitte); HACKIUS (Marc); FINSTERBUSCH (Jürgen); GERLOFF (Christian); FIEHLER (Jens); MÜNCHAU (Alexander)
AF :	Department of Neurology, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (1 aut., 3 aut., 5 aut., 7 aut.); Department of Neuroradiology, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (2 aut., 6 aut.); Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 3; Pp. 421-427; Bibl. 32 ref.
LA :	Anglais
EA :	It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2^*-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Pathologie du système nerveux; Encéphale; Fer; Ophtalmoplégie supranucléaire; Noyau gris central; Imagerie RMN
FG :	Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Syndrome oculomoteur; Pathologie de l'oeil; Syndrome du tronc cérébral
ED :	Parkinson disease; Nervous system diseases; Encephalon; Iron; Supranuclear ophthalmoplegia; Basal ganglion; Nuclear magnetic resonance imaging
EG :	Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Oculomotor syndrome; Eye disease; Brain stem syndrome
SD :	Parkinson enfermedad; Sistema nervioso patología; Encéfalo; Hierro; Oftalmoplejía supranuclear; Núcleo basal; Imaginería RMN
LO :	INIST-20953.354000506923350160
ID :	12-0198680

Links to Exploration step

Pascal:12-0198680

Le document en format XML

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<keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term>
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<front><div type="abstract" xml:lang="en">It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2<sup>*</sup>
-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.</div>
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<s3>DEU</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA20><s1>421-427</s1>
</fA20>
<fA21><s1>2012</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>32 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>12-0198680</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
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<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2<sup>*</sup>
-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
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<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Fer</s0>
<s2>NC</s2>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Iron</s0>
<s2>NC</s2>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Hierro</s0>
<s2>NC</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Ophtalmoplégie supranucléaire</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Supranuclear ophthalmoplegia</s0>
<s5>11</s5>
</fC03>
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<s5>11</s5>
</fC03>
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<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>12</s5>
</fC03>
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<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Nuclear magnetic resonance imaging</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Imaginería RMN</s0>
<s5>13</s5>
</fC03>
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<s5>37</s5>
</fC07>
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<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Syndrome oculomoteur</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Oculomotor syndrome</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Oculomotricidad síndrome</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie de l'oeil</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Eye disease</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Ojo patología</s0>
<s5>44</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Syndrome du tronc cérébral</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Brain stem syndrome</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Tallo encefalico sindrome</s0>
<s5>45</s5>
</fC07>
<fN21><s1>156</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
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<server><NO>PASCAL 12-0198680 INIST</NO>
<ET>Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy</ET>
<AU>BOELMANS (Kai); HOLST (Brigitte); HACKIUS (Marc); FINSTERBUSCH (Jürgen); GERLOFF (Christian); FIEHLER (Jens); MÜNCHAU (Alexander)</AU>
<AF>Department of Neurology, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (1 aut., 3 aut., 5 aut., 7 aut.); Department of Neuroradiology, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (2 aut., 6 aut.); Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf/Hamburg/Allemagne (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 3; Pp. 421-427; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>It can be difficult to clinically distinguish between classical Parkinson's disease (PD) and progressive supranuclear palsy. Previously, there have been no biomarkers that reliably allow this distinction to be made. We report that an abnormal brain iron accumulation is a marker for ongoing neurodegeneration in both conditions, but the conditions differ with respect to the anatomical distribution of these accumulations. We analyzed quantitative T2' maps as markers of regional brain iron content from PD and progressive supranuclear palsy patients and compared them to age-matched control subjects. T2-weighted and T2<sup>*</sup>
-weighted images were acquired in 30 PD patients, 12 progressive supranuclear palsy patients, and 24 control subjects at 1.5 Tesla. Mean T2' values were determined in regions-of-interest in the basal ganglia, thalamus, and white matter within each hemisphere. The main findings were shortened T2' values in the caudate nucleus, globus pallidus, and putamen in progressive supranuclear palsy compared to PD patients and controls. A stepwise linear discriminant analysis allowed progressive supranuclear palsy patients to be distinguished from PD patients and the healthy controls. All progressive supranuclear palsy patients were correctly classified. No progressive supranuclear palsy patient was classified as a healthy control, no healthy controls were incorrectly classified as having progressive supranuclear palsy, and only 6.7% of the PD patients were incorrectly classified as progressive supranuclear palsy. Regional decreases of T2' relaxation times in parts of the basal ganglia reflecting increased brain iron load in these areas are characteristic for progressive supranuclear palsy but not PD patients.</EA>
<CC>002B17; 002B17G</CC>
<FD>Maladie de Parkinson; Pathologie du   système nerveux; Encéphale; Fer; Ophtalmoplégie supranucléaire; Noyau gris central; Imagerie RMN</FD>
<FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central; Syndrome oculomoteur; Pathologie de l'oeil; Syndrome du tronc cérébral</FG>
<ED>Parkinson disease; Nervous system diseases; Encephalon; Iron; Supranuclear ophthalmoplegia; Basal ganglion; Nuclear magnetic resonance imaging</ED>
<EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Oculomotor syndrome; Eye disease; Brain stem syndrome</EG>
<SD>Parkinson enfermedad; Sistema nervioso patología; Encéfalo; Hierro; Oftalmoplejía supranuclear; Núcleo basal; Imaginería RMN</SD>
<LO>INIST-20953.354000506923350160</LO>
<ID>12-0198680</ID>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy

Brain Iron Deposition Fingerprints in Parkinson's Disease and Progressive Supranuclear Palsy

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