Serveur d'exploration sur la maladie de Parkinson

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease

Identifieur interne : 000105 ( Main/Exploration ); précédent : 000104; suivant : 000106

Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease

Auteurs : S. Orimo [Japon] ; T. Uchihara [Japon] ; T. Kanazawa [Japon] ; Y. Itoh [Japon] ; K. Wakabayashi ; A. Kakita [Japon] ; H. Takahashi [Japon]

Source :

RBID : ISTEX:FCDBC66B1FAC6602BEBCFDBC36CF406011460B6B

English descriptors

Abstract

S. Orimo, T. Uchihara, T. Kanazawa, Y. Itoh, K. Wakabayashi, A. Kakita and H. Takahashi (2011) Neuropathology and Applied Neurobiology37, 791–802 Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease Aims: We recently demonstrated accumulation of α‐synuclein aggregates of the cardiac sympathetic nerve in Parkinson's disease (PD) and a possible relationship between degeneration of the cardiac sympathetic nerve and α‐synuclein aggregates. The aim of this study is to determine whether there is a difference in the degenerative process between unmyelinated and myelinated axons of the cardiac nerve. Methods: We immunohistochemically examined cardiac tissues from four pathologically verified PD patients, nine patients with incidental Lewy body disease (ILBD) and five control subjects, using antibodies against neurofilament, myelin basic protein (MBP) and α‐synuclein. First, we counted the number of neurofilament‐immunoreactive axons not surrounded by MBP (unmyelinated axons) and those surrounded by MBP (myelinated axons). Next, we counted the number of unmyelinated and myelinated axons with α‐synuclein aggregates. Results: (i) The percentage of unmyelinated axons in PD (77.5 ± 9.14%) was significantly lower compared to that in control subjects (92.2 ± 2.40%). (ii) The ratio of unmyelinated axons with α‐synuclein aggregates to total axons with α‐synuclein aggregates in ILBD ranged from 94.4 to 100 (98.2 ± 2.18%). Among axons with α‐synuclein aggregates, unmyelinated axons were the overwhelming majority, comprising 98.2%. Conclusion: These findings suggest that in PD unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve, because α‐synuclein aggregates accumulate much more abundantly in unmyelinated axons.

Url:
DOI: 10.1111/j.1365-2990.2011.01194.x


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

<record>
<TEI wicri:istexFullTextTei="biblStruct">
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease</title>
<author>
<name sortKey="Orimo, S" sort="Orimo, S" uniqKey="Orimo S" first="S." last="Orimo">S. Orimo</name>
</author>
<author>
<name sortKey="Uchihara, T" sort="Uchihara, T" uniqKey="Uchihara T" first="T." last="Uchihara">T. Uchihara</name>
</author>
<author>
<name sortKey="Kanazawa, T" sort="Kanazawa, T" uniqKey="Kanazawa T" first="T." last="Kanazawa">T. Kanazawa</name>
</author>
<author>
<name sortKey="Itoh, Y" sort="Itoh, Y" uniqKey="Itoh Y" first="Y." last="Itoh">Y. Itoh</name>
</author>
<author>
<name sortKey="Wakabayashi, K" sort="Wakabayashi, K" uniqKey="Wakabayashi K" first="K." last="Wakabayashi">K. Wakabayashi</name>
</author>
<author>
<name sortKey="Kakita, A" sort="Kakita, A" uniqKey="Kakita A" first="A." last="Kakita">A. Kakita</name>
</author>
<author>
<name sortKey="Takahashi, H" sort="Takahashi, H" uniqKey="Takahashi H" first="H." last="Takahashi">H. Takahashi</name>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:FCDBC66B1FAC6602BEBCFDBC36CF406011460B6B</idno>
<date when="2011" year="2011">2011</date>
<idno type="doi">10.1111/j.1365-2990.2011.01194.x</idno>
<idno type="url">https://api.istex.fr/document/FCDBC66B1FAC6602BEBCFDBC36CF406011460B6B/fulltext/pdf</idno>
<idno type="wicri:Area/Main/Corpus">001386</idno>
<idno type="wicri:Area/Main/Curation">001174</idno>
<idno type="wicri:Area/Main/Exploration">000105</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title level="a" type="main" xml:lang="en">Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease</title>
<author>
<name sortKey="Orimo, S" sort="Orimo, S" uniqKey="Orimo S" first="S." last="Orimo">S. Orimo</name>
<affiliation wicri:level="3">
<country>Japon</country>
<placeName>
<settlement type="city">Tokyo</settlement>
</placeName>
<wicri:orgArea>Department of Neurology, Kanto Central Hospital</wicri:orgArea>
</affiliation>
<affiliation wicri:level="3">
<country>Japon</country>
<placeName>
<settlement type="city">Tokyo</settlement>
</placeName>
<wicri:orgArea>Department of Neurology, Tokyo Metropolitan Institute for Neuroscience</wicri:orgArea>
</affiliation>
</author>
<author>
<name sortKey="Uchihara, T" sort="Uchihara, T" uniqKey="Uchihara T" first="T." last="Uchihara">T. Uchihara</name>
<affiliation wicri:level="3">
<country>Japon</country>
<placeName>
<settlement type="city">Tokyo</settlement>
</placeName>
<wicri:orgArea>Department of Neurology, Tokyo Metropolitan Institute for Neuroscience</wicri:orgArea>
</affiliation>
</author>
<author>
<name sortKey="Kanazawa, T" sort="Kanazawa, T" uniqKey="Kanazawa T" first="T." last="Kanazawa">T. Kanazawa</name>
<affiliation wicri:level="3">
<country>Japon</country>
<placeName>
<settlement type="city">Tokyo</settlement>
</placeName>
<wicri:orgArea>Department of Neurology, Tokyo Metropolitan Institute for Neuroscience</wicri:orgArea>
</affiliation>
</author>
<author>
<name sortKey="Itoh, Y" sort="Itoh, Y" uniqKey="Itoh Y" first="Y." last="Itoh">Y. Itoh</name>
<affiliation wicri:level="3">
<country>Japon</country>
<placeName>
<settlement type="city">Tokyo</settlement>
</placeName>
<wicri:orgArea>Department of Internal Medicine, Yokufukai Geriatric Hospital</wicri:orgArea>
</affiliation>
</author>
<author>
<name sortKey="Wakabayashi, K" sort="Wakabayashi, K" uniqKey="Wakabayashi K" first="K." last="Wakabayashi">K. Wakabayashi</name>
<affiliation>
<wicri:noCountry code="subField">Hirosaki</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Kakita, A" sort="Kakita, A" uniqKey="Kakita A" first="A." last="Kakita">A. Kakita</name>
<affiliation wicri:level="1">
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Pathology, Brain Research Institute, University of Niigata, Graduate School of Medicine, Niigata</wicri:regionArea>
<wicri:noRegion>Niigata</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Takahashi, H" sort="Takahashi, H" uniqKey="Takahashi H" first="H." last="Takahashi">H. Takahashi</name>
<affiliation wicri:level="1">
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Pathology, Brain Research Institute, University of Niigata, Graduate School of Medicine, Niigata</wicri:regionArea>
<wicri:noRegion>Niigata</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">Neuropathology and Applied Neurobiology</title>
<idno type="ISSN">0305-1846</idno>
<idno type="eISSN">1365-2990</idno>
<imprint>
<publisher>Blackwell Publishing Ltd</publisher>
<pubPlace>Oxford, UK</pubPlace>
<date type="published" when="2011-12">2011-12</date>
<biblScope unit="volume">37</biblScope>
<biblScope unit="issue">7</biblScope>
<biblScope unit="page" from="791">791</biblScope>
<biblScope unit="page" to="802">802</biblScope>
</imprint>
<idno type="ISSN">0305-1846</idno>
</series>
<idno type="istex">FCDBC66B1FAC6602BEBCFDBC36CF406011460B6B</idno>
<idno type="DOI">10.1111/j.1365-2990.2011.01194.x</idno>
<idno type="ArticleID">NAN1194</idno>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0305-1846</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Parkinson's disease</term>
<term>cardiac sympathetic nerve</term>
<term>incidental Lewy body disease</term>
<term>myelinated axon</term>
<term>unmyelinated axon</term>
<term>α‐synuclein</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">S. Orimo, T. Uchihara, T. Kanazawa, Y. Itoh, K. Wakabayashi, A. Kakita and H. Takahashi (2011) Neuropathology and Applied Neurobiology37, 791–802 Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease Aims: We recently demonstrated accumulation of α‐synuclein aggregates of the cardiac sympathetic nerve in Parkinson's disease (PD) and a possible relationship between degeneration of the cardiac sympathetic nerve and α‐synuclein aggregates. The aim of this study is to determine whether there is a difference in the degenerative process between unmyelinated and myelinated axons of the cardiac nerve. Methods: We immunohistochemically examined cardiac tissues from four pathologically verified PD patients, nine patients with incidental Lewy body disease (ILBD) and five control subjects, using antibodies against neurofilament, myelin basic protein (MBP) and α‐synuclein. First, we counted the number of neurofilament‐immunoreactive axons not surrounded by MBP (unmyelinated axons) and those surrounded by MBP (myelinated axons). Next, we counted the number of unmyelinated and myelinated axons with α‐synuclein aggregates. Results: (i) The percentage of unmyelinated axons in PD (77.5 ± 9.14%) was significantly lower compared to that in control subjects (92.2 ± 2.40%). (ii) The ratio of unmyelinated axons with α‐synuclein aggregates to total axons with α‐synuclein aggregates in ILBD ranged from 94.4 to 100 (98.2 ± 2.18%). Among axons with α‐synuclein aggregates, unmyelinated axons were the overwhelming majority, comprising 98.2%. Conclusion: These findings suggest that in PD unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve, because α‐synuclein aggregates accumulate much more abundantly in unmyelinated axons.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Japon</li>
</country>
<settlement>
<li>Tokyo</li>
</settlement>
</list>
<tree>
<noCountry>
<name sortKey="Wakabayashi, K" sort="Wakabayashi, K" uniqKey="Wakabayashi K" first="K." last="Wakabayashi">K. Wakabayashi</name>
</noCountry>
<country name="Japon">
<noRegion>
<name sortKey="Orimo, S" sort="Orimo, S" uniqKey="Orimo S" first="S." last="Orimo">S. Orimo</name>
</noRegion>
<name sortKey="Itoh, Y" sort="Itoh, Y" uniqKey="Itoh Y" first="Y." last="Itoh">Y. Itoh</name>
<name sortKey="Kakita, A" sort="Kakita, A" uniqKey="Kakita A" first="A." last="Kakita">A. Kakita</name>
<name sortKey="Kanazawa, T" sort="Kanazawa, T" uniqKey="Kanazawa T" first="T." last="Kanazawa">T. Kanazawa</name>
<name sortKey="Orimo, S" sort="Orimo, S" uniqKey="Orimo S" first="S." last="Orimo">S. Orimo</name>
<name sortKey="Takahashi, H" sort="Takahashi, H" uniqKey="Takahashi H" first="H." last="Takahashi">H. Takahashi</name>
<name sortKey="Uchihara, T" sort="Uchihara, T" uniqKey="Uchihara T" first="T." last="Uchihara">T. Uchihara</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000105 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000105 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    ParkinsonV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:FCDBC66B1FAC6602BEBCFDBC36CF406011460B6B
   |texte=   Unmyelinated axons are more vulnerable to degeneration than myelinated axons of the cardiac nerve in Parkinson's disease
}}

Wicri

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 18:06:51 2016. Site generation: Wed Mar 6 18:46:03 2024