Movement Disorders (revue)

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Brain Stem Pathology in Parkinson's Disease: An Evaluation of the Braak Staging Model

Identifieur interne : 000B83 ( PascalFrancis/Checkpoint ); précédent : 000B82; suivant : 000B84

Brain Stem Pathology in Parkinson's Disease: An Evaluation of the Braak Staging Model

Auteurs : Ann E. Kingsbury [Royaume-Uni] ; Rina Bandopadhyay [Royaume-Uni] ; Laura Silveira-Moriyama [Royaume-Uni] ; Hilary Ayling [Royaume-Uni] ; Constantinos Kallis [Royaume-Uni] ; William Sterlacci [Autriche] ; Hans Maeir [Autriche] ; Werner Poewe [Autriche] ; Andrew Lees (neurologue) [Royaume-Uni]

Source :

RBID : Pascal:10-0512928

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Abstract

The lower brain stem of 25 pathologically-confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy-type α-synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically-normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo-rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another.


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Pascal:10-0512928

Le document en format XML

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<div type="abstract" xml:lang="en">The lower brain stem of 25 pathologically-confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy-type α-synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically-normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo-rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another.</div>
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<s1>Department of Pathology, Innsbruck Medical University</s1>
<s2>Innsbruck</s2>
<s3>AUT</s3>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="04">
<s1>Queen Square Brain Bank for Neurological Disorders, UCL, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA20>
<s1>2508-2515</s1>
</fA20>
<fA21>
<s1>2010</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>20953</s2>
<s5>354000191411680050</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>31 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>10-0512928</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Movement disorders</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>The lower brain stem of 25 pathologically-confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy-type α-synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically-normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo-rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another.</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>
<fC03 i1="02" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<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>Tronc cérébral</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Brain stem</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Tronco cerebral</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Anatomopathologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Anatomic pathology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Anatomía patológica</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Evaluation</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Evaluation</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Evaluación</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Modèle</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Models</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Modelo</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Corps Lewy</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Lewy body</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Cuerpo Lewy</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Bulbe rachidien</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Medulla oblongata</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Bulbo raquídeo</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Noyau dorsal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Dorsal nucleus</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Núcleo dorsal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Noyau moteur</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Motor nucleus</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Núcleo motor</s0>
<s5>16</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Encephalon</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21>
<s1>347</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Autriche</li>
<li>Royaume-Uni</li>
</country>
<region>
<li>Angleterre</li>
<li>Grand Londres</li>
<li>Tyrol (Land)</li>
</region>
<settlement>
<li>Innsbruck</li>
<li>Londres</li>
</settlement>
<orgName>
<li>National Hospital for Neurology and Neurosurgery</li>
<li>Université de médecine d'Innsbruck</li>
</orgName>
</list>
<tree>
<country name="Royaume-Uni">
<region name="Angleterre">
<name sortKey="Kingsbury, Ann E" sort="Kingsbury, Ann E" uniqKey="Kingsbury A" first="Ann E." last="Kingsbury">Ann E. Kingsbury</name>
</region>
<name sortKey="Ayling, Hilary" sort="Ayling, Hilary" uniqKey="Ayling H" first="Hilary" last="Ayling">Hilary Ayling</name>
<name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name>
<name sortKey="Kallis, Constantinos" sort="Kallis, Constantinos" uniqKey="Kallis C" first="Constantinos" last="Kallis">Constantinos Kallis</name>
<name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name>
<name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name>
<name sortKey="Silveira Moriyama, Laura" sort="Silveira Moriyama, Laura" uniqKey="Silveira Moriyama L" first="Laura" last="Silveira-Moriyama">Laura Silveira-Moriyama</name>
</country>
<country name="Autriche">
<noRegion>
<name sortKey="Sterlacci, William" sort="Sterlacci, William" uniqKey="Sterlacci W" first="William" last="Sterlacci">William Sterlacci</name>
</noRegion>
<name sortKey="Maeir, Hans" sort="Maeir, Hans" uniqKey="Maeir H" first="Hans" last="Maeir">Hans Maeir</name>
<name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name>
</country>
</tree>
</affiliations>
</record>

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