Movement Disorders (revue)

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Torpedoes in Parkinson's disease, Alzheimer's disease, essential tremor, and control brains

Identifieur interne : 001761 ( Istex/Corpus ); précédent : 001760; suivant : 001762

Torpedoes in Parkinson's disease, Alzheimer's disease, essential tremor, and control brains

Auteurs : Elan D. Louis ; Phyllis L. Faust ; Jean-Paul G. Vonsattel ; Lawrence S. Honig ; Alex Rajput ; Ali Rajput ; Rajesh Pahwa ; Kelly E. Lyons ; Webster G. Ross ; Rodger J. Elble ; Cordelia Erickson-Davis ; Carol B. Moskowitz ; Arlene Lawton

Source :

RBID : ISTEX:54859E4773EED91D39BC5617891C483D915E5ABE

English descriptors

Abstract

Purkinje cell axonal swellings (“torpedoes”), described in several cerebellar disorders as well as essential tremor (ET), have not been quantified in common neurodegenerative conditions. The aim of this study was to quantify torpedoes Parkinson's disease (PD) and Alzheimer's disease (AD) compared with ET and control brains. Brains included 40 ET cases (34 cerebellar ET, 6 Lewy body variant of ET) and age‐matched comparison brains (21 AD, 14 PD/diffuse Lewy body disease, 25 controls). Torpedoes were counted in 20 × 25 mm cerebellar cortical sections stained with Luxol Fast Blue/Hematoxylin and Eosin. The median number of torpedoes in cerebellar ET (12) was 12× higher than that of controls (1) and nearly 2.5× higher than in AD (5) or PD/DLBD (5) (all P ≤ 0.005). Furthermore, in a logistic regression model that adjusted for age and Alzheimer's‐type changes, each torpedo more than doubled the odds of having cerebellar ET (Odds ratiocerebellar ET vs. control = 2.57, P = 0.006), indicating that the association between increased torpedoes and cerebellar ET was independent of these Alzheimer's‐type changes. Although torpedoes are increased in AD and PD, as well as cerebellar ET, the magnitude of increase in cerebellar ET is greater, and cannot be accounted for by concomitant AD or PD pathology. © 2009 Movement Disorder Society

Url:
DOI: 10.1002/mds.22567

Links to Exploration step

ISTEX:54859E4773EED91D39BC5617891C483D915E5ABE

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<div type="abstract" xml:lang="fr">Purkinje cell axonal swellings (“torpedoes”), described in several cerebellar disorders as well as essential tremor (ET), have not been quantified in common neurodegenerative conditions. The aim of this study was to quantify torpedoes Parkinson's disease (PD) and Alzheimer's disease (AD) compared with ET and control brains. Brains included 40 ET cases (34 cerebellar ET, 6 Lewy body variant of ET) and age‐matched comparison brains (21 AD, 14 PD/diffuse Lewy body disease, 25 controls). Torpedoes were counted in 20 × 25 mm cerebellar cortical sections stained with Luxol Fast Blue/Hematoxylin and Eosin. The median number of torpedoes in cerebellar ET (12) was 12× higher than that of controls (1) and nearly 2.5× higher than in AD (5) or PD/DLBD (5) (all P ≤ 0.005). Furthermore, in a logistic regression model that adjusted for age and Alzheimer's‐type changes, each torpedo more than doubled the odds of having cerebellar ET (Odds ratiocerebellar ET vs. control = 2.57, P = 0.006), indicating that the association between increased torpedoes and cerebellar ET was independent of these Alzheimer's‐type changes. Although torpedoes are increased in AD and PD, as well as cerebellar ET, the magnitude of increase in cerebellar ET is greater, and cannot be accounted for by concomitant AD or PD pathology. © 2009 Movement Disorder Society</div>
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<abstract>Purkinje cell axonal swellings (“torpedoes”), described in several cerebellar disorders as well as essential tremor (ET), have not been quantified in common neurodegenerative conditions. The aim of this study was to quantify torpedoes Parkinson's disease (PD) and Alzheimer's disease (AD) compared with ET and control brains. Brains included 40 ET cases (34 cerebellar ET, 6 Lewy body variant of ET) and age‐matched comparison brains (21 AD, 14 PD/diffuse Lewy body disease, 25 controls). Torpedoes were counted in 20 × 25 mm cerebellar cortical sections stained with Luxol Fast Blue/Hematoxylin and Eosin. The median number of torpedoes in cerebellar ET (12) was 12× higher than that of controls (1) and nearly 2.5× higher than in AD (5) or PD/DLBD (5) (all P ≤ 0.005). Furthermore, in a logistic regression model that adjusted for age and Alzheimer's‐type changes, each torpedo more than doubled the odds of having cerebellar ET (Odds ratiocerebellar ET vs. control = 2.57, P = 0.006), indicating that the association between increased torpedoes and cerebellar ET was independent of these Alzheimer's‐type changes. Although torpedoes are increased in AD and PD, as well as cerebellar ET, the magnitude of increase in cerebellar ET is greater, and cannot be accounted for by concomitant AD or PD pathology. © 2009 Movement Disorder Society</abstract>
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<description>Correspondence: Unit 198, Neurological Institute, 710 West 168th Street, New York, NY 10032</description>
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<name type="personal">
<namePart type="given">Phyllis L.</namePart>
<namePart type="family">Faust</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
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</name>
<name type="personal">
<namePart type="given">Jean‐Paul G.</namePart>
<namePart type="family">Vonsattel</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<affiliation>Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
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</name>
<name type="personal">
<namePart type="given">Lawrence S.</namePart>
<namePart type="family">Honig</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<affiliation>Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
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</name>
<name type="personal">
<namePart type="given">Alex</namePart>
<namePart type="family">Rajput</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurology, Royal University Hospital, Saskatoon, Saskatchewan, Canada</affiliation>
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<name type="personal">
<namePart type="given">Ali</namePart>
<namePart type="family">Rajput</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurology, Royal University Hospital, Saskatoon, Saskatchewan, Canada</affiliation>
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<name type="personal">
<namePart type="given">Rajesh</namePart>
<namePart type="family">Pahwa</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas</affiliation>
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<name type="personal">
<namePart type="given">Kelly E.</namePart>
<namePart type="family">Lyons</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas</affiliation>
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<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Webster G.</namePart>
<namePart type="family">Ross</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Veterans Affairs Pacific Islands Health Care System, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii</affiliation>
<affiliation>Department of Medicine, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii</affiliation>
<affiliation>Department of Geriatrics, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii</affiliation>
<affiliation>Pacific Health Research Institute, Honolulu, Hawaii</affiliation>
<affiliation>Kuakini Medical Center/Honolulu‐Asia Aging Study, Honolulu, Hawaii</affiliation>
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<name type="personal">
<namePart type="given">Rodger J.</namePart>
<namePart type="family">Elble</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Department of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois</affiliation>
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</name>
<name type="personal">
<namePart type="given">Cordelia</namePart>
<namePart type="family">Erickson‐Davis</namePart>
<namePart type="termsOfAddress">BA</namePart>
<affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
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<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Carol B.</namePart>
<namePart type="family">Moskowitz</namePart>
<namePart type="termsOfAddress">MS</namePart>
<affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<affiliation>Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Arlene</namePart>
<namePart type="family">Lawton</namePart>
<namePart type="termsOfAddress">RN</namePart>
<affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
<affiliation>Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York</affiliation>
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<dateIssued encoding="w3cdtf">2009-08-15</dateIssued>
<dateCaptured encoding="w3cdtf">2008-11-07</dateCaptured>
<dateValid encoding="w3cdtf">2009-03-06</dateValid>
<copyrightDate encoding="w3cdtf">2009</copyrightDate>
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<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<abstract lang="fr">Purkinje cell axonal swellings (“torpedoes”), described in several cerebellar disorders as well as essential tremor (ET), have not been quantified in common neurodegenerative conditions. The aim of this study was to quantify torpedoes Parkinson's disease (PD) and Alzheimer's disease (AD) compared with ET and control brains. Brains included 40 ET cases (34 cerebellar ET, 6 Lewy body variant of ET) and age‐matched comparison brains (21 AD, 14 PD/diffuse Lewy body disease, 25 controls). Torpedoes were counted in 20 × 25 mm cerebellar cortical sections stained with Luxol Fast Blue/Hematoxylin and Eosin. The median number of torpedoes in cerebellar ET (12) was 12× higher than that of controls (1) and nearly 2.5× higher than in AD (5) or PD/DLBD (5) (all P ≤ 0.005). Furthermore, in a logistic regression model that adjusted for age and Alzheimer's‐type changes, each torpedo more than doubled the odds of having cerebellar ET (Odds ratiocerebellar ET vs. control = 2.57, P = 0.006), indicating that the association between increased torpedoes and cerebellar ET was independent of these Alzheimer's‐type changes. Although torpedoes are increased in AD and PD, as well as cerebellar ET, the magnitude of increase in cerebellar ET is greater, and cannot be accounted for by concomitant AD or PD pathology. © 2009 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: None.</note>
<note type="content">*The statistical analyses were conducted by Dr. Louis.</note>
<note type="funding">National Institutes of Health (Bethesda, MD) - No. R01 NS42859; No. P50 AG08702; No. P01 AG07232; </note>
<note type="funding">Parkinson's Disease Foundation (New York, NY)</note>
<note type="funding">Arlene Bronstein Essential Tremor Research Fund (Columbia University)</note>
<note type="funding">Claire O'Neil Essential Tremor Research Fund (Columbia University)</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>essential tremor</topic>
<topic>cerebellum</topic>
<topic>torpedoes</topic>
<topic>Parkinson's disease</topic>
<topic>pathology</topic>
<topic>Alzheimer's disease</topic>
</subject>
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<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>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>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>24</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>11</number>
</detail>
<extent unit="pages">
<start>1600</start>
<end>1605</end>
<total>6</total>
</extent>
</part>
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<identifier type="istex">54859E4773EED91D39BC5617891C483D915E5ABE</identifier>
<identifier type="DOI">10.1002/mds.22567</identifier>
<identifier type="ArticleID">MDS22567</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
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