Evidence for environmental causation of Parkinson's disease.
Identifieur interne : 002F76 ( Main/Exploration ); précédent : 002F75; suivant : 002F77Evidence for environmental causation of Parkinson's disease.
Auteurs : Raúl De La Fuente-Fernández [Canada] ; Donald B. CalneSource :
- Parkinsonism & related disorders [ 1353-8020 ] ; 2002.
English descriptors
- KwdEn :
- MESH :
- epidemiology : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease.
- Adult, Age of Onset, Aged, Environment, Female, Humans, Male, Middle Aged, Proportional Hazards Models.
Abstract
To address the question of whether Parkinson's disease (PD) is a genetic or an environmental disorder; (i) we modeled the hazard of PD using two-parameter hazard functions; and (ii) we investigated whether the hazard rate of index cases depended on the age of symptom onset in the affected parent (genetic model) or depended on the age of the index case at the time the affected parent developed PD (environmental model). We found that the hazard of PD increased monotonically with age according to a Weibull function. The risk associated with the presence of maternal PD did not depend on the age of onset of the affected mother but on the child's age at the time, the affected mother developed symptoms. The younger the child when the mother began to have symptoms, the higher the risk for the child. When the affected parent was the father, both models provided similar results. Whichever parent had PD, the age at onset of index cases correlated with their age at the time the affected parent developed PD, but not with the age of onset in the affected parent. Since the degree of environmental exposure shared by parents and children decreases as the child's age increases, these results indicate that PD is usually caused by an accumulation of transient environmental events. We provide evidence that this is not only true for sporadic cases but also for the majority of familial ones.
PubMed: 12039417
Affiliations:
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Le document en format XML
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Calne</name></author></analytic><series><title level="j">Parkinsonism & related disorders</title><idno type="ISSN">1353-8020</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Environment</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (epidemiology)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (genetics)</term><term>Proportional Hazards Models</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Environment</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Proportional Hazards Models</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To address the question of whether Parkinson's disease (PD) is a genetic or an environmental disorder; (i) we modeled the hazard of PD using two-parameter hazard functions; and (ii) we investigated whether the hazard rate of index cases depended on the age of symptom onset in the affected parent (genetic model) or depended on the age of the index case at the time the affected parent developed PD (environmental model). We found that the hazard of PD increased monotonically with age according to a Weibull function. The risk associated with the presence of maternal PD did not depend on the age of onset of the affected mother but on the child's age at the time, the affected mother developed symptoms. The younger the child when the mother began to have symptoms, the higher the risk for the child. When the affected parent was the father, both models provided similar results. Whichever parent had PD, the age at onset of index cases correlated with their age at the time the affected parent developed PD, but not with the age of onset in the affected parent. Since the degree of environmental exposure shared by parents and children decreases as the child's age increases, these results indicate that PD is usually caused by an accumulation of transient environmental events. We provide evidence that this is not only true for sporadic cases but also for the majority of familial ones.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B" last="Calne">Donald B. Calne</name></noCountry><country name="Canada"><noRegion><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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