Segregation analysis of Parkinson disease
Identifieur interne : 001E61 ( Main/Exploration ); précédent : 001E60; suivant : 001E62Segregation analysis of Parkinson disease
Auteurs : Sepideh Zareparsi [États-Unis] ; Todd D. Taylor [États-Unis] ; Emily L. Harris [États-Unis] ; Haydeh Payami [États-Unis]Source :
- American Journal of Medical Genetics [ 0148-7299 ] ; 1998-12-04.
English descriptors
- KwdEn :
Abstract
Parkinson disease (PD) is a prevalent movement disorder of unknown cause whose incidence rises with increasing age. Nearly 20% of PD is familial, a small subset of which exhibits autosomal dominant transmission. However, in most families, the inheritance is not clear. To determine the most likely mode of inheritance of PD, we performed complex segregation analyses using kindreds of 136 PD patients randomly ascertained from a clinic population. The hypotheses of a nontransmissible environmental factor, no major gene or type (sporadic), and all Mendelian inheritance (dominant, recessive, additive, decreasing) were rejected (P <0.001). Familial clustering of PD in this data set is best explained by a rare familial factor which a) is transmitted in a non‐Mendelian fashion, and b) influences the age at onset of PD. If confirmed, our results have immediate implications in gene‐mapping studies which often search for genes that behave in a Mendelian fashion that affect susceptibility rather than age at onset and long term implications in understanding the pathogenesis of PD. Am. J. Med. Genet. 80:410–417, 1998. © 1998 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1096-8628(19981204)80:4<410::AID-AJMG21>3.0.CO;2-2
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Segregation analysis of Parkinson disease</title><author><name sortKey="Zareparsi, Sepideh" sort="Zareparsi, Sepideh" uniqKey="Zareparsi S" first="Sepideh" last="Zareparsi">Sepideh Zareparsi</name></author><author><name sortKey="Taylor, Todd D" sort="Taylor, Todd D" uniqKey="Taylor T" first="Todd D." last="Taylor">Todd D. Taylor</name></author><author><name sortKey="Harris, Emily L" sort="Harris, Emily L" uniqKey="Harris E" first="Emily L." last="Harris">Emily L. Harris</name></author><author><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:ED32249EA240E4A2E07D754272021B538047D514</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/(SICI)1096-8628(19981204)80:4<410::AID-AJMG21>3.0.CO;2-2</idno><idno type="url">https://api.istex.fr/document/ED32249EA240E4A2E07D754272021B538047D514/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000F96</idno><idno type="wicri:Area/Main/Curation">000E11</idno><idno type="wicri:Area/Main/Exploration">001E61</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Segregation analysis of Parkinson disease</title><author><name sortKey="Zareparsi, Sepideh" sort="Zareparsi, Sepideh" uniqKey="Zareparsi S" first="Sepideh" last="Zareparsi">Sepideh Zareparsi</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland</wicri:cityArea></affiliation></author><author><name sortKey="Taylor, Todd D" sort="Taylor, Todd D" uniqKey="Taylor T" first="Todd D." last="Taylor">Todd D. Taylor</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland</wicri:cityArea></affiliation></author><author><name sortKey="Harris, Emily L" sort="Harris, Emily L" uniqKey="Harris E" first="Emily L." last="Harris">Emily L. Harris</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Public Health and Preventive Medicine, Oregon Health Sciences University, Portland</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Kaiser Permanente Center for Health Research, Portland</wicri:cityArea></affiliation></author><author><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Department of Neurology, Oregon Health Sciences University, Portland</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">American Journal of Medical Genetics</title><title level="j" type="abbrev">Am. J. Med. Genet.</title><idno type="ISSN">0148-7299</idno><idno type="eISSN">1096-8628</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1998-12-04">1998-12-04</date><biblScope unit="volume">80</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="410">410</biblScope><biblScope unit="page" to="417">417</biblScope></imprint><idno type="ISSN">0148-7299</idno></series><idno type="istex">ED32249EA240E4A2E07D754272021B538047D514</idno><idno type="DOI">10.1002/(SICI)1096-8628(19981204)80:4<410::AID-AJMG21>3.0.CO;2-2</idno><idno type="ArticleID">AJMG21</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0148-7299</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson disease</term><term>age at onset</term><term>genetics</term><term>mode of inheritance</term><term>segregation analysis</term><term>susceptibility</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease (PD) is a prevalent movement disorder of unknown cause whose incidence rises with increasing age. Nearly 20% of PD is familial, a small subset of which exhibits autosomal dominant transmission. However, in most families, the inheritance is not clear. To determine the most likely mode of inheritance of PD, we performed complex segregation analyses using kindreds of 136 PD patients randomly ascertained from a clinic population. The hypotheses of a nontransmissible environmental factor, no major gene or type (sporadic), and all Mendelian inheritance (dominant, recessive, additive, decreasing) were rejected (P <0.001). Familial clustering of PD in this data set is best explained by a rare familial factor which a) is transmitted in a non‐Mendelian fashion, and b) influences the age at onset of PD. If confirmed, our results have immediate implications in gene‐mapping studies which often search for genes that behave in a Mendelian fashion that affect susceptibility rather than age at onset and long term implications in understanding the pathogenesis of PD. Am. J. Med. Genet. 80:410–417, 1998. © 1998 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Oregon</li></region></list><tree><country name="États-Unis"><region name="Oregon"><name sortKey="Zareparsi, Sepideh" sort="Zareparsi, Sepideh" uniqKey="Zareparsi S" first="Sepideh" last="Zareparsi">Sepideh Zareparsi</name></region><name sortKey="Harris, Emily L" sort="Harris, Emily L" uniqKey="Harris E" first="Emily L." last="Harris">Emily L. Harris</name><name sortKey="Harris, Emily L" sort="Harris, Emily L" uniqKey="Harris E" first="Emily L." last="Harris">Emily L. Harris</name><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><name sortKey="Taylor, Todd D" sort="Taylor, Todd D" uniqKey="Taylor T" first="Todd D." last="Taylor">Todd D. Taylor</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001E61 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001E61 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:ED32249EA240E4A2E07D754272021B538047D514
|texte= Segregation analysis of Parkinson disease
}}
| This area was generated with Dilib version V0.6.23. |  |