A mathematical model of pathogenesis in idiopathic parkinsonism.
Identifieur interne : 001965 ( PubMed/Corpus ); précédent : 001964; suivant : 001966A mathematical model of pathogenesis in idiopathic parkinsonism.
Auteurs : M. Schulzer ; C S Lee ; E K Mak ; F J Vingerhoets ; D B CalneSource :
- Brain : a journal of neurology [ 0006-8950 ] ; 1994.
English descriptors
- KwdEn :
- MESH :
- etiology : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Adult, Aged, Aging, Algorithms, Humans, Middle Aged, Models, Theoretical.
Abstract
We used our observations relating clinical deficits in idiopathic parkinsonism (IP) to age and to disease duration (Lee et al, Brain 1994; 117: 501-7), to develop a mathematical model of the temporal profile of neurodegeneration in IP. We also examined other sets of relevant published observations and applied three additional assumptions which permitted the formulation of this model. Our model indicates that accelerating or decelerating processes should be excluded as the driving forces behind neuronal death in IP. Mechanisms in accord with the model include: (i) an event that kills some neurons and damages others in such a way that their life expectation is reduced; or (ii) an event that starts a process which is continuously killing healthy neurons at a constant rate. The model enables us to extrapolate back to estimate when the causal event occurred. It also explains why IP proceeds more rapidly in older patients. The model has potential relevance to other neurodegenerative disorders, such as Alzheimer's disease and amyotrophic lateral sclerosis.
PubMed: 8032861
Links to Exploration step
pubmed:8032861Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A mathematical model of pathogenesis in idiopathic parkinsonism.</title><author><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name><affiliation><nlm:affiliation>Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, C S" sort="Lee, C S" uniqKey="Lee C" first="C S" last="Lee">C S Lee</name></author><author><name sortKey="Mak, E K" sort="Mak, E K" uniqKey="Mak E" first="E K" last="Mak">E K Mak</name></author><author><name sortKey="Vingerhoets, F J" sort="Vingerhoets, F J" uniqKey="Vingerhoets F" first="F J" last="Vingerhoets">F J Vingerhoets</name></author><author><name sortKey="Calne, D B" sort="Calne, D B" uniqKey="Calne D" first="D B" last="Calne">D B Calne</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:8032861</idno><idno type="pmid">8032861</idno><idno type="wicri:Area/PubMed/Corpus">001965</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001965</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A mathematical model of pathogenesis in idiopathic parkinsonism.</title><author><name sortKey="Schulzer, M" sort="Schulzer, M" uniqKey="Schulzer M" first="M" last="Schulzer">M. Schulzer</name><affiliation><nlm:affiliation>Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, C S" sort="Lee, C S" uniqKey="Lee C" first="C S" last="Lee">C S Lee</name></author><author><name sortKey="Mak, E K" sort="Mak, E K" uniqKey="Mak E" first="E K" last="Mak">E K Mak</name></author><author><name sortKey="Vingerhoets, F J" sort="Vingerhoets, F J" uniqKey="Vingerhoets F" first="F J" last="Vingerhoets">F J Vingerhoets</name></author><author><name sortKey="Calne, D B" sort="Calne, D B" uniqKey="Calne D" first="D B" last="Calne">D B Calne</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aging</term><term>Algorithms</term><term>Humans</term><term>Middle Aged</term><term>Models, Theoretical</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><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>Adult</term><term>Aged</term><term>Aging</term><term>Algorithms</term><term>Humans</term><term>Middle Aged</term><term>Models, Theoretical</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We used our observations relating clinical deficits in idiopathic parkinsonism (IP) to age and to disease duration (Lee et al, Brain 1994; 117: 501-7), to develop a mathematical model of the temporal profile of neurodegeneration in IP. We also examined other sets of relevant published observations and applied three additional assumptions which permitted the formulation of this model. Our model indicates that accelerating or decelerating processes should be excluded as the driving forces behind neuronal death in IP. Mechanisms in accord with the model include: (i) an event that kills some neurons and damages others in such a way that their life expectation is reduced; or (ii) an event that starts a process which is continuously killing healthy neurons at a constant rate. The model enables us to extrapolate back to estimate when the causal event occurred. It also explains why IP proceeds more rapidly in older patients. The model has potential relevance to other neurodegenerative disorders, such as Alzheimer's disease and amyotrophic lateral sclerosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8032861</PMID><DateCreated><Year>1994</Year><Month>08</Month><Day>18</Day></DateCreated><DateCompleted><Year>1994</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8950</ISSN><JournalIssue CitedMedium="Print"><Volume>117 ( Pt 3)</Volume><PubDate><Year>1994</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>A mathematical model of pathogenesis in idiopathic parkinsonism.</ArticleTitle><Pagination><MedlinePgn>509-16</MedlinePgn></Pagination><Abstract><AbstractText>We used our observations relating clinical deficits in idiopathic parkinsonism (IP) to age and to disease duration (Lee et al, Brain 1994; 117: 501-7), to develop a mathematical model of the temporal profile of neurodegeneration in IP. We also examined other sets of relevant published observations and applied three additional assumptions which permitted the formulation of this model. Our model indicates that accelerating or decelerating processes should be excluded as the driving forces behind neuronal death in IP. Mechanisms in accord with the model include: (i) an event that kills some neurons and damages others in such a way that their life expectation is reduced; or (ii) an event that starts a process which is continuously killing healthy neurons at a constant rate. The model enables us to extrapolate back to estimate when the causal event occurred. It also explains why IP proceeds more rapidly in older patients. The model has potential relevance to other neurodegenerative disorders, such as Alzheimer's disease and amyotrophic lateral sclerosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schulzer</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>C S</ForeName><Initials>CS</Initials></Author><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>E K</ForeName><Initials>EK</Initials></Author><Author ValidYN="Y"><LastName>Vingerhoets</LastName><ForeName>F J</ForeName><Initials>FJ</Initials></Author><Author ValidYN="Y"><LastName>Calne</LastName><ForeName>D B</ForeName><Initials>DB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="Y">Aging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008962" MajorTopicYN="Y">Models, Theoretical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1994</Year><Month>6</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1994</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1994</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8032861</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001965 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001965 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:8032861
|texte= A mathematical model of pathogenesis in idiopathic parkinsonism.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:8032861" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |