Modelling idiopathic Parkinson disease as a complex illness can inform incidence rate in healthy adults: the PR EDIGT score.
Identifieur interne : 000052 ( PubMed/Checkpoint ); précédent : 000051; suivant : 000053Modelling idiopathic Parkinson disease as a complex illness can inform incidence rate in healthy adults: the PR EDIGT score.
Auteurs : Michael G. Schlossmacher [Canada] ; Julianna J. Tomlinson [Canada] ; Goncalo Santos [Canada] ; Bojan Shutinoski [Canada] ; Earl G. Brown [Canada] ; Douglas Manuel [Canada] ; Tiago Mestre [Canada]Source :
- The European journal of neuroscience [ 1460-9568 ] ; 2017.
Abstract
Fifty-five years after the concept of dopamine replacement therapy was introduced, Parkinson disease (PD) remains an incurable neurological disorder. To date, no disease-modifying therapeutic has been approved. The inability to predict PD incidence risk in healthy adults is seen as a limitation in drug development, because by the time of clinical diagnosis ≥ 60% of dopamine neurons have been lost. We have designed an incidence prediction model founded on the concept that the pathogenesis of PD is similar to that of many disorders observed in ageing humans, i.e. a complex, multifactorial disease. Our model considers five factors to determine cumulative incidence rates for PD in healthy adults: (i) DNA variants that alter susceptibility (D), e.g. carrying a LRRK2 or GBA risk allele; (ii) Exposure history to select environmental factors including xenobiotics (E); (iii) Gene-environment interactions that initiate pathological tissue responses (I), e.g. a rise in ROS levels, misprocessing of amyloidogenic proteins (foremost, α-synuclein) and dysregulated inflammation; (iv) sex (or gender; G); and importantly, (v) time (T) encompassing ageing-related changes, latency of illness and propagation of disease. We propose that cumulative incidence rates for PD (PR ) can be calculated in healthy adults, using the formula: PR (%) = (E + D + I) × G × T. Here, we demonstrate six case scenarios leading to young-onset parkinsonism (n = 3) and late-onset PD (n = 3). Further development and validation of this prediction model and its scoring system promise to improve subject recruitment in future intervention trials. Such efforts will be aimed at disease prevention through targeted selection of healthy individuals with a higher prediction score for developing PD in the future and at disease modification in subjects that already manifest prodromal signs.
DOI: 10.1111/ejn.13476
PubMed: 27859866
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Schlossmacher</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Tomlinson, Julianna J" sort="Tomlinson, Julianna J" uniqKey="Tomlinson J" first="Julianna J" last="Tomlinson">Julianna J. Tomlinson</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Santos, Goncalo" sort="Santos, Goncalo" uniqKey="Santos G" first="Goncalo" last="Santos">Goncalo Santos</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Medicine, University of Ottawa, Ottawa</wicri:regionArea><wicri:noRegion>Ottawa</wicri:noRegion></affiliation></author><author><name sortKey="Shutinoski, Bojan" sort="Shutinoski, Bojan" uniqKey="Shutinoski B" first="Bojan" last="Shutinoski">Bojan Shutinoski</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Brown, Earl G" sort="Brown, Earl G" uniqKey="Brown E" first="Earl G" last="Brown">Earl G. Brown</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Manuel, Douglas" sort="Manuel, Douglas" uniqKey="Manuel D" first="Douglas" last="Manuel">Douglas Manuel</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Medicine, University of Ottawa, Ottawa</wicri:regionArea><wicri:noRegion>Ottawa</wicri:noRegion></affiliation></author><author><name sortKey="Mestre, Tiago" sort="Mestre, Tiago" uniqKey="Mestre T" first="Tiago" last="Mestre">Tiago Mestre</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5</wicri:regionArea><wicri:noRegion>K1H 8M5</wicri:noRegion></affiliation></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="eISSN">1460-9568</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fifty-five years after the concept of dopamine replacement therapy was introduced, Parkinson disease (PD) remains an incurable neurological disorder. To date, no disease-modifying therapeutic has been approved. The inability to predict PD incidence risk in healthy adults is seen as a limitation in drug development, because by the time of clinical diagnosis ≥ 60% of dopamine neurons have been lost. We have designed an incidence prediction model founded on the concept that the pathogenesis of PD is similar to that of many disorders observed in ageing humans, i.e. a complex, multifactorial disease. Our model considers five factors to determine cumulative incidence rates for PD in healthy adults: (i) DNA variants that alter susceptibility (D), e.g. carrying a LRRK2 or GBA risk allele; (ii) Exposure history to select environmental factors including xenobiotics (E); (iii) Gene-environment interactions that initiate pathological tissue responses (I), e.g. a rise in ROS levels, misprocessing of amyloidogenic proteins (foremost, α-synuclein) and dysregulated inflammation; (iv) sex (or gender; G); and importantly, (v) time (T) encompassing ageing-related changes, latency of illness and propagation of disease. We propose that cumulative incidence rates for PD (PR ) can be calculated in healthy adults, using the formula: PR (%) = (E + D + I) × G × T. Here, we demonstrate six case scenarios leading to young-onset parkinsonism (n = 3) and late-onset PD (n = 3). Further development and validation of this prediction model and its scoring system promise to improve subject recruitment in future intervention trials. Such efforts will be aimed at disease prevention through targeted selection of healthy individuals with a higher prediction score for developing PD in the future and at disease modification in subjects that already manifest prodromal signs.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27859866</PMID><DateCreated><Year>2016</Year><Month>11</Month><Day>18</Day></DateCreated><DateRevised><Year>2017</Year><Month>03</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-9568</ISSN><JournalIssue CitedMedium="Internet"><Volume>45</Volume><Issue>1</Issue><PubDate><Year>2017</Year><Month>Jan</Month></PubDate></JournalIssue><Title>The European journal of neuroscience</Title><ISOAbbreviation>Eur. J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Modelling idiopathic Parkinson disease as a complex illness can inform incidence rate in healthy adults: the PR EDIGT score.</ArticleTitle><Pagination><MedlinePgn>175-191</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/ejn.13476</ELocationID><Abstract><AbstractText>Fifty-five years after the concept of dopamine replacement therapy was introduced, Parkinson disease (PD) remains an incurable neurological disorder. To date, no disease-modifying therapeutic has been approved. The inability to predict PD incidence risk in healthy adults is seen as a limitation in drug development, because by the time of clinical diagnosis ≥ 60% of dopamine neurons have been lost. We have designed an incidence prediction model founded on the concept that the pathogenesis of PD is similar to that of many disorders observed in ageing humans, i.e. a complex, multifactorial disease. Our model considers five factors to determine cumulative incidence rates for PD in healthy adults: (i) DNA variants that alter susceptibility (D), e.g. carrying a LRRK2 or GBA risk allele; (ii) Exposure history to select environmental factors including xenobiotics (E); (iii) Gene-environment interactions that initiate pathological tissue responses (I), e.g. a rise in ROS levels, misprocessing of amyloidogenic proteins (foremost, α-synuclein) and dysregulated inflammation; (iv) sex (or gender; G); and importantly, (v) time (T) encompassing ageing-related changes, latency of illness and propagation of disease. We propose that cumulative incidence rates for PD (PR ) can be calculated in healthy adults, using the formula: PR (%) = (E + D + I) × G × T. Here, we demonstrate six case scenarios leading to young-onset parkinsonism (n = 3) and late-onset PD (n = 3). Further development and validation of this prediction model and its scoring system promise to improve subject recruitment in future intervention trials. Such efforts will be aimed at disease prevention through targeted selection of healthy individuals with a higher prediction score for developing PD in the future and at disease modification in subjects that already manifest prodromal signs.</AbstractText><CopyrightInformation>© 2016 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schlossmacher</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Neurology, Department of Medicine, The Ottawa Hospital, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Ottawa Brain & Mind Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tomlinson</LastName><ForeName>Julianna J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Ottawa Brain & Mind Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Santos</LastName><ForeName>Goncalo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shutinoski</LastName><ForeName>Bojan</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Ottawa Brain & Mind Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>Earl G</ForeName><Initials>EG</Initials><AffiliationInfo><Affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manuel</LastName><ForeName>Douglas</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mestre</LastName><ForeName>Tiago</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Neuroscience Program, Ottawa Hospital Research Institute, 451 Smyth Road, RGH #1414, Ottawa, ON, K1H 8M5, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division of Neurology, Department of Medicine, The Ottawa Hospital, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University of Ottawa Brain & Mind Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Faculty of Medicine, University of Ottawa, Ottawa, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate 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MajorTopicYN="N">probability</Keyword><Keyword MajorTopicYN="N">toxin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>08</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>10</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>11</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>11</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27859866</ArticleId><ArticleId IdType="doi">10.1111/ejn.13476</ArticleId><ArticleId IdType="pmc">PMC5324667</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G" last="Schlossmacher">Michael G. Schlossmacher</name></noRegion><name sortKey="Brown, Earl G" sort="Brown, Earl G" uniqKey="Brown E" first="Earl G" last="Brown">Earl G. Brown</name><name sortKey="Manuel, Douglas" sort="Manuel, Douglas" uniqKey="Manuel D" first="Douglas" last="Manuel">Douglas Manuel</name><name sortKey="Mestre, Tiago" sort="Mestre, Tiago" uniqKey="Mestre T" first="Tiago" last="Mestre">Tiago Mestre</name><name sortKey="Santos, Goncalo" sort="Santos, Goncalo" uniqKey="Santos G" first="Goncalo" last="Santos">Goncalo Santos</name><name sortKey="Shutinoski, Bojan" sort="Shutinoski, Bojan" uniqKey="Shutinoski B" first="Bojan" last="Shutinoski">Bojan Shutinoski</name><name sortKey="Tomlinson, Julianna J" sort="Tomlinson, Julianna J" uniqKey="Tomlinson J" first="Julianna J" last="Tomlinson">Julianna J. Tomlinson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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