Quantification of Cerebellar Hemispheric Purkinje Cell Linear Density: 32 ET Cases vs. 16 Controls
Identifieur interne : 000081 ( Pmc/Checkpoint ); précédent : 000080; suivant : 000082Quantification of Cerebellar Hemispheric Purkinje Cell Linear Density: 32 ET Cases vs. 16 Controls
Auteurs : Elan D. Louis [États-Unis] ; Rachel Babij [États-Unis] ; Michelle Lee [États-Unis] ; Etty Cortés [États-Unis] ; Jean-Paul G. Vonsattel [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2013.
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 vs. 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 16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31 per 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.
Url:
DOI: 10.1002/mds.25629
PubMed: 23925732
PubMed Central: 3830681
Affiliations:
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">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 vs. controls.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">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<sup>−1</sup>
Purkinje cell layer.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Purkinje cell linear density was lower in 32 ET cases than 16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31 per mm<sup>−1</sup>
, p = 0.03). Purkinje cell linear density was inversely associated with torpedo count (r = −0.38, p = 0.028).</p>
</sec>
<sec id="S4"><title>Discussion</title>
<p id="P4">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.</p>
</sec>
</div>
</front>
</TEI>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Quantification of Cerebellar Hemispheric Purkinje Cell Linear Density: 32 ET Cases vs. 16 Controls</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Louis</surname>
<given-names>Elan D.</given-names>
</name>
<degrees>MD MSc</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="aff" rid="A3">3</xref>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Babij</surname>
<given-names>Rachel</given-names>
</name>
<degrees>BS</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lee</surname>
<given-names>Michelle</given-names>
</name>
<degrees>BA</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cortés</surname>
<given-names>Etty</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Vonsattel</surname>
<given-names>Jean-Paul G.</given-names>
</name>
<degrees>MD</degrees>
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<aff id="A1"><label>1</label>
GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA.</aff>
<aff id="A2"><label>2</label>
Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, NY, USA.</aff>
<aff id="A3"><label>3</label>
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, USA.</aff>
<aff id="A4"><label>4</label>
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.</aff>
<aff id="A5"><label>5</label>
Department of Pathology and Cell Biology, Columbia University Medical Center and the New York Presbyterian Hospital, New York, NY, USA.</aff>
<author-notes><corresp id="CR1"><bold>Correspondence:</bold>
Dr. Elan Louis, Unit 198, Neurological Institute, 710 West 168<sup>th</sup>
Street, New York, NY, 10032, USA. Tel: (212) 305 – 9194, FAX: (212) 305 -1304, <email>EDL2@columbia.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>21</day>
<month>8</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>07</day>
<month>8</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><month>11</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>11</month>
<year>2014</year>
</pub-date>
<volume>28</volume>
<issue>13</issue>
<elocation-id>10.1002/mds.25629</elocation-id>
<abstract><sec id="S1"><title>Background</title>
<p id="P1">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 vs. controls.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">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<sup>−1</sup>
Purkinje cell layer.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">Purkinje cell linear density was lower in 32 ET cases than 16 controls (1.14 ± 0.32 vs. 1.35 ± 0.31 per mm<sup>−1</sup>
, p = 0.03). Purkinje cell linear density was inversely associated with torpedo count (r = −0.38, p = 0.028).</p>
</sec>
<sec id="S4"><title>Discussion</title>
<p id="P4">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.</p>
</sec>
</abstract>
<kwd-group><kwd>essential tremor</kwd>
<kwd>Purkinje cell</kwd>
<kwd>cerebellum</kwd>
<kwd>brain</kwd>
<kwd>pathology</kwd>
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<funding-group><award-group><funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source>
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