Quantification of cerebellar hemispheric purkinje cell linear density: 32 ET cases versus 16 controls.
Identifieur interne : 000795 ( PubMed/Curation ); précédent : 000794; suivant : 000796Quantification of cerebellar hemispheric purkinje cell linear density: 32 ET cases versus 16 controls.
Auteurs : Elan D. Louis [États-Unis] ; Rachel Babij ; Michelle Lee ; Etty Cortés ; Jean-Paul G. VonsattelSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Calbindin 1.
- metabolism : Purkinje Cells.
- pathology : Cerebellum, Essential Tremor, Purkinje Cells.
- Aged, Aged, 80 and over, Cell Count, Female, Functional Laterality, Humans, Male, Statistics, Nonparametric.
Abstract
Although essential tremor (ET) is among the most prevalent neurological diseases, its precise pathogenesis is not understood. Purkinje cell loss has been observed in some studies and is the focus of interest and debate. Expressing these data as Purkinje cells/layer length allows one to adjust for the inherent curved nature of the cerebellar folia. Capitalizing on the Essential Tremor Centralized Brain Repository, we quantified Purkinje cell linear density in cases versus controls. Free-floating 100-μm parasagittal cerebellar hemispheric sections were subjected to rabbit polyclonal anti-Calbindin D28k antibody, and 10 random fields/brain were selected for quantification of Purkinje cells/mm(-1) Purkinje cell layer. Purkinje cell linear density was lower in 32 ET cases than in16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31/mm(-1) , P = 0.03). Purkinje cell linear density was inversely associated with torpedo count (r = -0.38, P = 0.028). The current sample of ET cases demonstrates a reduction in Purkinje cell number relative to that of controls. Greater Purkinje cell axonal remodeling (torpedoes) was found in individuals who had the most Purkinje cell drop out. The role of Purkinje cell loss in the pathogenesis of this disorder merits additional study.
DOI: 10.1002/mds.25629
PubMed: 23925732
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Louis</name><affiliation wicri:level="1"><nlm:affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York</wicri:regionArea></affiliation></author><author><name sortKey="Babij, Rachel" sort="Babij, Rachel" uniqKey="Babij R" first="Rachel" last="Babij">Rachel Babij</name></author><author><name sortKey="Lee, Michelle" sort="Lee, Michelle" uniqKey="Lee M" first="Michelle" last="Lee">Michelle Lee</name></author><author><name sortKey="Cortes, Etty" sort="Cortes, Etty" uniqKey="Cortes E" first="Etty" last="Cortés">Etty Cortés</name></author><author><name sortKey="Vonsattel, Jean Paul G" sort="Vonsattel, Jean Paul G" uniqKey="Vonsattel J" first="Jean-Paul G" last="Vonsattel">Jean-Paul G. 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Louis</name><affiliation wicri:level="1"><nlm:affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York</wicri:regionArea></affiliation></author><author><name sortKey="Babij, Rachel" sort="Babij, Rachel" uniqKey="Babij R" first="Rachel" last="Babij">Rachel Babij</name></author><author><name sortKey="Lee, Michelle" sort="Lee, Michelle" uniqKey="Lee M" first="Michelle" last="Lee">Michelle Lee</name></author><author><name sortKey="Cortes, Etty" sort="Cortes, Etty" uniqKey="Cortes E" first="Etty" last="Cortés">Etty Cortés</name></author><author><name sortKey="Vonsattel, Jean Paul G" sort="Vonsattel, Jean Paul G" uniqKey="Vonsattel J" first="Jean-Paul G" last="Vonsattel">Jean-Paul G. Vonsattel</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Calbindin 1 (metabolism)</term><term>Cell Count</term><term>Cerebellum (pathology)</term><term>Essential Tremor (pathology)</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Purkinje Cells (metabolism)</term><term>Purkinje Cells (pathology)</term><term>Statistics, Nonparametric</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calbindin 1</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Purkinje Cells</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebellum</term><term>Essential Tremor</term><term>Purkinje Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Count</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Statistics, Nonparametric</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although essential tremor (ET) is among the most prevalent neurological diseases, its precise pathogenesis is not understood. Purkinje cell loss has been observed in some studies and is the focus of interest and debate. Expressing these data as Purkinje cells/layer length allows one to adjust for the inherent curved nature of the cerebellar folia. Capitalizing on the Essential Tremor Centralized Brain Repository, we quantified Purkinje cell linear density in cases versus controls. Free-floating 100-μm parasagittal cerebellar hemispheric sections were subjected to rabbit polyclonal anti-Calbindin D28k antibody, and 10 random fields/brain were selected for quantification of Purkinje cells/mm(-1) Purkinje cell layer. Purkinje cell linear density was lower in 32 ET cases than in16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31/mm(-1) , P = 0.03). Purkinje cell linear density was inversely associated with torpedo count (r = -0.38, P = 0.028). The current sample of ET cases demonstrates a reduction in Purkinje cell number relative to that of controls. Greater Purkinje cell axonal remodeling (torpedoes) was found in individuals who had the most Purkinje cell drop out. The role of Purkinje cell loss in the pathogenesis of this disorder merits additional study.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23925732</PMID><DateCreated><Year>2013</Year><Month>11</Month><Day>14</Day></DateCreated><DateCompleted><Year>2014</Year><Month>06</Month><Day>27</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>13</Issue><PubDate><Year>2013</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Quantification of cerebellar hemispheric purkinje cell linear density: 32 ET cases versus 16 controls.</ArticleTitle><Pagination><MedlinePgn>1854-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25629</ELocationID><Abstract><AbstractText>Although essential tremor (ET) is among the most prevalent neurological diseases, its precise pathogenesis is not understood. Purkinje cell loss has been observed in some studies and is the focus of interest and debate. Expressing these data as Purkinje cells/layer length allows one to adjust for the inherent curved nature of the cerebellar folia. Capitalizing on the Essential Tremor Centralized Brain Repository, we quantified Purkinje cell linear density in cases versus controls. Free-floating 100-μm parasagittal cerebellar hemispheric sections were subjected to rabbit polyclonal anti-Calbindin D28k antibody, and 10 random fields/brain were selected for quantification of Purkinje cells/mm(-1) Purkinje cell layer. Purkinje cell linear density was lower in 32 ET cases than in16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31/mm(-1) , P = 0.03). Purkinje cell linear density was inversely associated with torpedo count (r = -0.38, P = 0.028). The current sample of ET cases demonstrates a reduction in Purkinje cell number relative to that of controls. Greater Purkinje cell axonal remodeling (torpedoes) was found in individuals who had the most Purkinje cell drop out. The role of Purkinje cell loss in the pathogenesis of this disorder merits additional study.</AbstractText><CopyrightInformation>© 2013 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Louis</LastName><ForeName>Elan D</ForeName><Initials>ED</Initials><AffiliationInfo><Affiliation>GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA; Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Babij</LastName><ForeName>Rachel</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Michelle</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Cortés</LastName><ForeName>Etty</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Vonsattel</LastName><ForeName>Jean-Paul G</ForeName><Initials>JP</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS042859</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS042859</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>08</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064092">Calbindin 1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Alcohol Clin Exp Res. 2001 Feb;25(2):228-35</RefSource><PMID Version="1">11236837</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2012 Sep;18(8):1003-4</RefSource><PMID Version="1">22795481</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 2003 Mar-Apr;24(2):197-211</RefSource><PMID Version="1">12498954</PMID></CommentsCorrections><CommentsCorrections 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Version="1">21252587</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 2011 Sep;82(9):1038-40</RefSource><PMID Version="1">20802031</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cerebellum. 2011 Dec;10(4):812-9</RefSource><PMID Version="1">21656041</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurol. 2012 Apr;19(4):625-30</RefSource><PMID Version="1">22136494</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2012 Jun;18(5):626-8</RefSource><PMID Version="1">22306459</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2002 Nov 15;333(1):17-20</RefSource><PMID Version="1">12401550</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011689">Purkinje Cells</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018709">Statistics, Nonparametric</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS507707</OtherID><OtherID Source="NLM">PMC3830681</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Purkinje cell</Keyword><Keyword MajorTopicYN="N">brain</Keyword><Keyword MajorTopicYN="N">cerebellum</Keyword><Keyword MajorTopicYN="N">essential tremor</Keyword><Keyword MajorTopicYN="N">neurodegenerative</Keyword><Keyword MajorTopicYN="N">pathology</Keyword><Keyword MajorTopicYN="N">pathophysiology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>2</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>4</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>5</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2013</Year><Month>8</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>8</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>8</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>6</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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