The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.
Identifieur interne : 000F42 ( PubMed/Curation ); précédent : 000F41; suivant : 000F43The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.
Auteurs : Philippe Vernier [France] ; Frederic Moret ; Sophie Callier ; Marina Snapyan ; Christophe Wersinger ; Anita SidhuSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2004.
English descriptors
- KwdEn :
- Animals, Biological Evolution, Corpus Striatum (embryology), Corpus Striatum (metabolism), Corpus Striatum (pathology), Disease Models, Animal, Dopamine (metabolism), Humans, Nerve Degeneration (etiology), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Parkinson Disease (complications), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Dopamine.
- complications : Parkinson Disease.
- embryology : Corpus Striatum.
- etiology : Nerve Degeneration.
- metabolism : Corpus Striatum, Nerve Degeneration.
- pathology : Corpus Striatum, Nerve Degeneration, Parkinson Disease.
- physiopathology : Parkinson Disease.
- Animals, Biological Evolution, Disease Models, Animal, Humans.
Abstract
Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine-synthesizing cells of the mesostriatal-mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine-containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter--to name a few), which is not found in other dopamine-containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a-synuclein, parkin, and microtubule-associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT-dependent dopamine uptake, DAT-dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (alpha-synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.
DOI: 10.1196/annals.1332.015
PubMed: 15681811
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000F82
Links to Exploration step
pubmed:15681811Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.</title><author><name sortKey="Vernier, Philippe" sort="Vernier, Philippe" uniqKey="Vernier P" first="Philippe" last="Vernier">Philippe Vernier</name><affiliation wicri:level="1"><nlm:affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, Gif-sur-Yvette, France. vernier@iaf.cnrs-gif.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, Gif-sur-Yvette</wicri:regionArea></affiliation></author><author><name sortKey="Moret, Frederic" sort="Moret, Frederic" uniqKey="Moret F" first="Frederic" last="Moret">Frederic Moret</name></author><author><name sortKey="Callier, Sophie" sort="Callier, Sophie" uniqKey="Callier S" first="Sophie" last="Callier">Sophie Callier</name></author><author><name sortKey="Snapyan, Marina" sort="Snapyan, Marina" uniqKey="Snapyan M" first="Marina" last="Snapyan">Marina Snapyan</name></author><author><name sortKey="Wersinger, Christophe" sort="Wersinger, Christophe" uniqKey="Wersinger C" first="Christophe" last="Wersinger">Christophe Wersinger</name></author><author><name sortKey="Sidhu, Anita" sort="Sidhu, Anita" uniqKey="Sidhu A" first="Anita" last="Sidhu">Anita Sidhu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:15681811</idno><idno type="pmid">15681811</idno><idno type="doi">10.1196/annals.1332.015</idno><idno type="wicri:Area/PubMed/Corpus">000F82</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000F82</idno><idno type="wicri:Area/PubMed/Curation">000F42</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000F42</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.</title><author><name sortKey="Vernier, Philippe" sort="Vernier, Philippe" uniqKey="Vernier P" first="Philippe" last="Vernier">Philippe Vernier</name><affiliation wicri:level="1"><nlm:affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, Gif-sur-Yvette, France. vernier@iaf.cnrs-gif.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, Gif-sur-Yvette</wicri:regionArea></affiliation></author><author><name sortKey="Moret, Frederic" sort="Moret, Frederic" uniqKey="Moret F" first="Frederic" last="Moret">Frederic Moret</name></author><author><name sortKey="Callier, Sophie" sort="Callier, Sophie" uniqKey="Callier S" first="Sophie" last="Callier">Sophie Callier</name></author><author><name sortKey="Snapyan, Marina" sort="Snapyan, Marina" uniqKey="Snapyan M" first="Marina" last="Snapyan">Marina Snapyan</name></author><author><name sortKey="Wersinger, Christophe" sort="Wersinger, Christophe" uniqKey="Wersinger C" first="Christophe" last="Wersinger">Christophe Wersinger</name></author><author><name sortKey="Sidhu, Anita" sort="Sidhu, Anita" uniqKey="Sidhu A" first="Anita" last="Sidhu">Anita Sidhu</name></author></analytic><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Corpus Striatum (embryology)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Humans</term><term>Nerve Degeneration (etiology)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Disease Models, Animal</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine-synthesizing cells of the mesostriatal-mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine-containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter--to name a few), which is not found in other dopamine-containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a-synuclein, parkin, and microtubule-associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT-dependent dopamine uptake, DAT-dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (alpha-synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15681811</PMID><DateCreated><Year>2005</Year><Month>01</Month><Day>31</Day></DateCreated><DateCompleted><Year>2006</Year><Month>07</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0077-8923</ISSN><JournalIssue CitedMedium="Print"><Volume>1035</Volume><PubDate><Year>2004</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation></Journal><ArticleTitle>The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.</ArticleTitle><Pagination><MedlinePgn>231-49</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine-synthesizing cells of the mesostriatal-mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine-containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter--to name a few), which is not found in other dopamine-containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a-synuclein, parkin, and microtubule-associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT-dependent dopamine uptake, DAT-dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (alpha-synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vernier</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, Gif-sur-Yvette, France. vernier@iaf.cnrs-gif.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moret</LastName><ForeName>Frederic</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Callier</LastName><ForeName>Sophie</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Snapyan</LastName><ForeName>Marina</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Wersinger</LastName><ForeName>Christophe</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Sidhu</LastName><ForeName>Anita</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS-34914</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS-45326</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS041555</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann N Y Acad Sci</MedlineTA><NlmUniqueID>7506858</NlmUniqueID><ISSNLinking>0077-8923</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005075" MajorTopicYN="Y">Biological Evolution</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>58</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>2</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>7</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>2</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15681811</ArticleId><ArticleId IdType="pii">1035/1/231</ArticleId><ArticleId IdType="doi">10.1196/annals.1332.015</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000F42 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000F42 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:15681811
|texte= The degeneration of dopamine neurons in Parkinson's disease: insights from embryology and evolution of the mesostriatocortical system.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:15681811" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |