Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia.
Identifieur interne : 001415 ( Ncbi/Curation ); précédent : 001414; suivant : 001416Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia.
Auteurs : Nathan Pankratz [États-Unis] ; Lisa Byder ; Cheryl Halter ; Alice Rudolph ; Clifford W. Shults ; P Michael Conneally ; Tatiana Foroud ; William C. NicholsSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2006.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Aged, 80 and over, Alleles, Alzheimer Disease (genetics), Apolipoprotein E4, Apolipoproteins E (genetics), Female, Genotype, Heterozygote Detection, Homozygote, Humans, Lewy Body Disease (genetics), Male, Mental Status Schedule, Middle Aged, Neurologic Examination, Neuropsychological Tests, Parkinson Disease (genetics), Risk, Statistics as Topic, Survival Analysis.
- MESH :
- chemical , genetics : Apolipoproteins E.
- chemical : Apolipoprotein E4.
- genetics : Alzheimer Disease, Lewy Body Disease, Parkinson Disease.
- Adolescent, Adult, Aged, Aged, 80 and over, Alleles, Female, Genotype, Heterozygote Detection, Homozygote, Humans, Male, Mental Status Schedule, Middle Aged, Neurologic Examination, Neuropsychological Tests, Risk, Statistics as Topic, Survival Analysis.
Abstract
The epsilon4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one epsilon4 allele (OR=3.37; P=0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one epsilon4 allele (59.7 years) as compared with those homozygous for the more common epsilon3 allele (62.4 years; P=0.009). Thus, consistent with previous studies, we find evidence that the presence of an epsilon4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology.
DOI: 10.1002/mds.20663
PubMed: 16116614
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pubmed:16116614Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia.</title><author><name sortKey="Pankratz, Nathan" sort="Pankratz, Nathan" uniqKey="Pankratz N" first="Nathan" last="Pankratz">Nathan Pankratz</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author><author><name sortKey="Byder, Lisa" sort="Byder, Lisa" uniqKey="Byder L" first="Lisa" last="Byder">Lisa Byder</name></author><author><name sortKey="Halter, Cheryl" sort="Halter, Cheryl" uniqKey="Halter C" first="Cheryl" last="Halter">Cheryl Halter</name></author><author><name sortKey="Rudolph, Alice" sort="Rudolph, Alice" uniqKey="Rudolph A" first="Alice" last="Rudolph">Alice Rudolph</name></author><author><name sortKey="Shults, Clifford W" sort="Shults, Clifford W" uniqKey="Shults C" first="Clifford W" last="Shults">Clifford W. Shults</name></author><author><name sortKey="Conneally, P Michael" sort="Conneally, P Michael" uniqKey="Conneally P" first="P Michael" last="Conneally">P Michael Conneally</name></author><author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name></author><author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William C" last="Nichols">William C. Nichols</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="doi">10.1002/mds.20663</idno><idno type="RBID">pubmed:16116614</idno><idno type="pmid">16116614</idno><idno type="wicri:Area/PubMed/Corpus">002E97</idno><idno type="wicri:Area/PubMed/Curation">002E97</idno><idno type="wicri:Area/PubMed/Checkpoint">002B54</idno><idno type="wicri:Area/Ncbi/Merge">001415</idno><idno type="wicri:Area/Ncbi/Curation">001415</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia.</title><author><name sortKey="Pankratz, Nathan" sort="Pankratz, Nathan" uniqKey="Pankratz N" first="Nathan" last="Pankratz">Nathan Pankratz</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author><author><name sortKey="Byder, Lisa" sort="Byder, Lisa" uniqKey="Byder L" first="Lisa" last="Byder">Lisa Byder</name></author><author><name sortKey="Halter, Cheryl" sort="Halter, Cheryl" uniqKey="Halter C" first="Cheryl" last="Halter">Cheryl Halter</name></author><author><name sortKey="Rudolph, Alice" sort="Rudolph, Alice" uniqKey="Rudolph A" first="Alice" last="Rudolph">Alice Rudolph</name></author><author><name sortKey="Shults, Clifford W" sort="Shults, Clifford W" uniqKey="Shults C" first="Clifford W" last="Shults">Clifford W. Shults</name></author><author><name sortKey="Conneally, P Michael" sort="Conneally, P Michael" uniqKey="Conneally P" first="P Michael" last="Conneally">P Michael Conneally</name></author><author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name></author><author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William C" last="Nichols">William C. Nichols</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Alzheimer Disease (genetics)</term><term>Apolipoprotein E4</term><term>Apolipoproteins E (genetics)</term><term>Female</term><term>Genotype</term><term>Heterozygote Detection</term><term>Homozygote</term><term>Humans</term><term>Lewy Body Disease (genetics)</term><term>Male</term><term>Mental Status Schedule</term><term>Middle Aged</term><term>Neurologic Examination</term><term>Neuropsychological Tests</term><term>Parkinson Disease (genetics)</term><term>Risk</term><term>Statistics as Topic</term><term>Survival Analysis</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoproteins E</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Apolipoprotein E4</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Alzheimer Disease</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Alleles</term><term>Female</term><term>Genotype</term><term>Heterozygote Detection</term><term>Homozygote</term><term>Humans</term><term>Male</term><term>Mental Status Schedule</term><term>Middle Aged</term><term>Neurologic Examination</term><term>Neuropsychological Tests</term><term>Risk</term><term>Statistics as Topic</term><term>Survival Analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The epsilon4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one epsilon4 allele (OR=3.37; P=0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one epsilon4 allele (59.7 years) as compared with those homozygous for the more common epsilon3 allele (62.4 years; P=0.009). Thus, consistent with previous studies, we find evidence that the presence of an epsilon4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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