Alpha-synuclein is not a requisite component of synaptic boutons in the adult human central nervous system
Identifieur interne : 001C63 ( Main/Exploration ); précédent : 001C62; suivant : 001C64Alpha-synuclein is not a requisite component of synaptic boutons in the adult human central nervous system
Auteurs : Heiko Braak [Allemagne] ; Kelly Del Tredici [Allemagne] ; Wei Ping Gai [Australie] ; Eva Braak [Allemagne]Source :
- Journal of Chemical Neuroanatomy [ 0891-0618 ] ; 2000.
English descriptors
Abstract
It is increasingly clear that the normal protein α-synuclein is in some manner closely associated with presynaptic components of select neuronal types within the adult human central nervous system (CNS) and, in addition, that in its pathologically altered state α-synuclein aggregates selectively in the form of filamentous inclusion bodies during certain progressive neurodegenerative disorders, such as familial and sporadic Parkinson's disease. By having the antibody AFshp raised specifically to α-synuclein to label Parkinson disease-specific Lewy bodies and Lewy neurites as well as synaptic boutons containing the unaltered protein, an initial attempt is made to map the overall distribution pattern and describe the staining behavior of the immunoreactive punctae in select regions of the prosencephalon. Neocortical immunolabeling is most prominent in the prodigious, but incompletely myelinated, association fields and faintest in the heavily myelinated primary motor and primary sensory fields, with the premotor and first order sensory association areas occupying an intermediate position. Of the thalamic grays evaluated, those containing powerfully myelinated fiber tracts (e.g. centrum medianum, habenular complex) show the weakest immunolabeling, whereas, less sturdily myelinated structures are highly immunoreactive. The fact that the immunostaining spectrum for normal α-synuclein is so broad, together with the fact that some thalamic sites actually are immunonegative leads to the following conclusions (1) α-synuclein, although present in the synaptic boutons of many nerve cells in the adult human CNS, is by no means ubiquitous there, and (2) neuronal types lacking the normal protein cannot generate the Parkinson's disease-specific filamentous pathology.
Url:
DOI: 10.1016/S0891-0618(00)00101-0
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Alpha-synuclein is not a requisite component of synaptic boutons in the adult human central nervous system</title><author><name sortKey="Braak, Heiko" sort="Braak, Heiko" uniqKey="Braak H" first="Heiko" last="Braak">Heiko Braak</name></author><author><name sortKey="Tredici, Kelly Del" sort="Tredici, Kelly Del" uniqKey="Tredici K" first="Kelly Del" last="Tredici">Kelly Del Tredici</name></author><author><name sortKey="Gai, Wei Ping" sort="Gai, Wei Ping" uniqKey="Gai W" first="Wei Ping" last="Gai">Wei Ping Gai</name></author><author><name sortKey="Braak, Eva" sort="Braak, Eva" uniqKey="Braak E" first="Eva" last="Braak">Eva Braak</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:13922AE87E26D023D3041FD6815353A081ADC4DD</idno><date when="2000" year="2000">2000</date><idno type="doi">10.1016/S0891-0618(00)00101-0</idno><idno type="url">https://api.istex.fr/document/13922AE87E26D023D3041FD6815353A081ADC4DD/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002275</idno><idno type="wicri:Area/Main/Curation">001F60</idno><idno type="wicri:Area/Main/Exploration">001C63</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Alpha-synuclein is not a requisite component of synaptic boutons in the adult human central nervous system</title><author><name sortKey="Braak, Heiko" sort="Braak, Heiko" uniqKey="Braak H" first="Heiko" last="Braak">Heiko Braak</name><affiliation wicri:level="1"><country wicri:rule="url">Allemagne</country></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Clinical Neuroanatomy, J.W. Goethe University, Theodor Stern Kai 7, D-60590 Frankfurt</wicri:regionArea><wicri:noRegion>60590 Frankfurt</wicri:noRegion><wicri:noRegion>D-60590 Frankfurt</wicri:noRegion></affiliation></author><author><name sortKey="Tredici, Kelly Del" sort="Tredici, Kelly Del" uniqKey="Tredici K" first="Kelly Del" last="Tredici">Kelly Del Tredici</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Clinical Neuroanatomy, J.W. Goethe University, Theodor Stern Kai 7, D-60590 Frankfurt</wicri:regionArea><wicri:noRegion>60590 Frankfurt</wicri:noRegion><wicri:noRegion>D-60590 Frankfurt</wicri:noRegion></affiliation></author><author><name sortKey="Gai, Wei Ping" sort="Gai, Wei Ping" uniqKey="Gai W" first="Wei Ping" last="Gai">Wei Ping Gai</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Physiology, Flinders Medical Centre, Bedford Park, SA 5042</wicri:regionArea><wicri:noRegion>SA 5042</wicri:noRegion></affiliation></author><author><name sortKey="Braak, Eva" sort="Braak, Eva" uniqKey="Braak E" first="Eva" last="Braak">Eva Braak</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Clinical Neuroanatomy, J.W. Goethe University, Theodor Stern Kai 7, D-60590 Frankfurt</wicri:regionArea><wicri:noRegion>60590 Frankfurt</wicri:noRegion><wicri:noRegion>D-60590 Frankfurt</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Chemical Neuroanatomy</title><title level="j" type="abbrev">CHENEU</title><idno type="ISSN">0891-0618</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">3–4</biblScope><biblScope unit="page" from="245">245</biblScope><biblScope unit="page" to="252">252</biblScope></imprint><idno type="ISSN">0891-0618</idno></series><idno type="istex">13922AE87E26D023D3041FD6815353A081ADC4DD</idno><idno type="DOI">10.1016/S0891-0618(00)00101-0</idno><idno type="PII">S0891-0618(00)00101-0</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0891-0618</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>Presynaptic boutons</term><term>Selective vulnerability</term><term>Synuclein family</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is increasingly clear that the normal protein α-synuclein is in some manner closely associated with presynaptic components of select neuronal types within the adult human central nervous system (CNS) and, in addition, that in its pathologically altered state α-synuclein aggregates selectively in the form of filamentous inclusion bodies during certain progressive neurodegenerative disorders, such as familial and sporadic Parkinson's disease. By having the antibody AFshp raised specifically to α-synuclein to label Parkinson disease-specific Lewy bodies and Lewy neurites as well as synaptic boutons containing the unaltered protein, an initial attempt is made to map the overall distribution pattern and describe the staining behavior of the immunoreactive punctae in select regions of the prosencephalon. Neocortical immunolabeling is most prominent in the prodigious, but incompletely myelinated, association fields and faintest in the heavily myelinated primary motor and primary sensory fields, with the premotor and first order sensory association areas occupying an intermediate position. Of the thalamic grays evaluated, those containing powerfully myelinated fiber tracts (e.g. centrum medianum, habenular complex) show the weakest immunolabeling, whereas, less sturdily myelinated structures are highly immunoreactive. The fact that the immunostaining spectrum for normal α-synuclein is so broad, together with the fact that some thalamic sites actually are immunonegative leads to the following conclusions (1) α-synuclein, although present in the synaptic boutons of many nerve cells in the adult human CNS, is by no means ubiquitous there, and (2) neuronal types lacking the normal protein cannot generate the Parkinson's disease-specific filamentous pathology.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Braak, Heiko" sort="Braak, Heiko" uniqKey="Braak H" first="Heiko" last="Braak">Heiko Braak</name></noRegion><name sortKey="Braak, Eva" sort="Braak, Eva" uniqKey="Braak E" first="Eva" last="Braak">Eva Braak</name><name sortKey="Braak, Heiko" sort="Braak, Heiko" uniqKey="Braak H" first="Heiko" last="Braak">Heiko Braak</name><name sortKey="Tredici, Kelly Del" sort="Tredici, Kelly Del" uniqKey="Tredici K" first="Kelly Del" last="Tredici">Kelly Del Tredici</name></country><country name="Australie"><noRegion><name sortKey="Gai, Wei Ping" sort="Gai, Wei Ping" uniqKey="Gai W" first="Wei Ping" last="Gai">Wei Ping Gai</name></noRegion></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 001C63 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001C63 | 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:13922AE87E26D023D3041FD6815353A081ADC4DD
|texte= Alpha-synuclein is not a requisite component of synaptic boutons in the adult human central nervous system
}}
| This area was generated with Dilib version V0.6.23. |  |