A mathematical model of pathogenesis in idiopathic parkinsonism
Identifieur interne : 001195 ( Istex/Corpus ); précédent : 001194; suivant : 001196A mathematical model of pathogenesis in idiopathic parkinsonism
Auteurs : M. Schulzer ; C. S. Lee ; E. K. Mak ; F. J. G. Vingerhoets ; D. B. CalneSource :
- Brain [ 0006-8950 ] ; 1994-06.
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 amyotophic lateral sclerosis.
Url:
DOI: 10.1093/brain/117.3.509
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Schulzer</name><affiliation><mods:affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</mods: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><affiliation><mods:affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</mods:affiliation></affiliation></author><author><name sortKey="Mak, E K" sort="Mak, E K" uniqKey="Mak E" first="E. K." last="Mak">E. K. 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Calne</name><affiliation><mods:affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1994-06">1994-06</date><biblScope unit="volume">117</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="509">509</biblScope><biblScope unit="page" to="516">516</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="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 amyotophic lateral sclerosis.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>M. 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B. Calne, Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">A mathematical model of pathogenesis in idiopathic parkinsonism</title><author xml:id="author-0000"><persName><forename type="first">M.</forename><surname>Schulzer</surname></persName><affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</affiliation></author><author xml:id="author-0001"><persName><forename type="first">C. S.</forename><surname>Lee</surname></persName><affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</affiliation></author><author xml:id="author-0002"><persName><forename type="first">E. K.</forename><surname>Mak</surname></persName><affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</affiliation></author><author xml:id="author-0003"><persName><forename type="first">F. J. G.</forename><surname>Vingerhoets</surname></persName><affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</affiliation></author><author xml:id="author-0004"><persName><forename type="first">D. 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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. 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S.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Mak</surname><given-names>E. K.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Vingerhoets</surname><given-names>F. J. G.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Calne</surname><given-names>D. B.</given-names></name><xref ref-type="corresp" rid="cor1"></xref></contrib><aff><institution>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia</institution> <addr-line>Canada</addr-line></aff></contrib-group><author-notes><corresp id="cor1">Correspondence to: Dr D. B. Calne, Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5</corresp></author-notes><pub-date pub-type="ppub"><month>6</month><year>1994</year></pub-date><volume>117</volume><issue>3</issue><fpage>509</fpage><lpage>516</lpage><history><date date-type="received"><day>29</day><month>6</month><year>1993</year></date><date date-type="rev-recd"><day>24</day><month>1</month><year>1994</year></date><date date-type="accepted"><day>08</day><month>2</month><year>1994</year></date></history><copyright-statement>© Oxford University Press</copyright-statement><copyright-year>1994</copyright-year><abstract><p>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 amyotophic lateral sclerosis.</p></abstract><kwd-group><kwd>Parkinson's disease</kwd><kwd>natural history</kwd><kwd>pathogenesis</kwd><kwd>ageing</kwd><kwd>mathematical model</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>A mathematical model of pathogenesis in idiopathic parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>A mathematical model of pathogenesis in idiopathic parkinsonism</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Schulzer</namePart><affiliation>Neurodegenerative Disorders Centre, Division of Neurology, Department of Medicine, Vancouver Hospital and Health Sciences Centre, University of British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. 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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 amyotophic lateral sclerosis.</abstract><note type="author-notes">Correspondence to: Dr D. B. Calne, Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Purdy Pavilion, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5</note><subject><genre>keywords</genre><topic>Parkinson's disease</topic><topic>natural history</topic><topic>pathogenesis</topic><topic>ageing</topic><topic>mathematical model</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>117</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>509</start><end>516</end></extent></part></relatedItem><identifier type="istex">FA3EED9C1B64F37F1A5AB77E24196ADD5729B30C</identifier><identifier type="DOI">10.1093/brain/117.3.509</identifier><identifier type="ArticleID">117.3.509</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/FA3EED9C1B64F37F1A5AB77E24196ADD5729B30C/annexes/pdf</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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