BuChE‐K and APOE ϵ4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline
Identifieur interne : 002417 ( Main/Exploration ); précédent : 002416; suivant : 002418BuChE‐K and APOE ϵ4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline
Auteurs : Roger Lane [États-Unis] ; Yunsheng He [États-Unis] ; Christopher Morris [Royaume-Uni] ; James B. Leverenz [États-Unis] ; Murat Emre [Turquie] ; Clive Ballard [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-02-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Apolipoprotein E, Apolipoprotein E4 (genetics), Butyrylcholinesterase (genetics), Cognition Disorders (diagnosis), Cognition Disorders (epidemiology), Cognitive disorder, Female, Gene Frequency, Genotype, Humans, Hyperhomocysteinemia, Hyperhomocysteinemia (epidemiology), Lewy Body Disease (drug therapy), Lewy Body Disease (epidemiology), Lewy Body Disease (genetics), Lewy body dementia, Male, Nervous system diseases, Neuroprotective Agents (therapeutic use), Neuropsychological Tests, Parkinson disease, Parkinson's disease dementia, Phenylcarbamates (therapeutic use), Psychomotor Disorders (diagnosis), Psychomotor Disorders (epidemiology), Randomized Controlled Trials as Topic, Severity of Illness Index, apolipoprotein E, butyrylcholinesterase, dementia with Lewy bodies.
- MESH :
- chemical , genetics : Apolipoprotein E4, Butyrylcholinesterase.
- diagnosis : Cognition Disorders, Psychomotor Disorders.
- drug therapy : Lewy Body Disease.
- epidemiology : Cognition Disorders, Hyperhomocysteinemia, Lewy Body Disease, Psychomotor Disorders.
- genetics : Lewy Body Disease.
- chemical , therapeutic use : Neuroprotective Agents, Phenylcarbamates.
- Aged, Female, Gene Frequency, Genotype, Humans, Male, Neuropsychological Tests, Randomized Controlled Trials as Topic, Severity of Illness Index.
Abstract
Apolipoprotein E (APOE) ε4 and butyrylcholinesterase‐K (BuChE‐K) are associated with an increased risk for Alzheimer's disease. The primary objective was to evaluate frequencies of these alleles in dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). A secondary objective was to evaluate influences on rate of cognitive decline. This analysis used data from participants consenting to pharmacogenetic testing in placebo‐controlled rivastigmine studies. Allele frequencies in DLB and PDD were compared using logistic regression. Within the PDD placebo sample, associations with cognitive decline were evaluated (the DLB sample was too small for these evaluations). Fifty‐seven DLB and 323 PDD subjects provided APOE and BuChE data. Allelic frequencies were higher in DLB, relative to PDD subjects, for BuChE‐K (P = 0.06), APOE ε4 (P < 0.001), or both alleles together (P < 0.001). More rapid cognitive decline was seen in PDD patients carrying both alleles, compared with other genotypes. Subjects with hyperhomocysteinemia were associated with more rapid decline in the presence of BuChE‐K, with or without APOE ε4. These results suggest that genetic and biochemical risk factors for AD and PDD pathology may be important in dementia onset and progression in these Lewy body disorders. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22357
Affiliations:
- Royaume-Uni, Turquie, États-Unis
- Angleterre, Grand Londres, Massachusetts, New Jersey, Washington (État)
- Londres, Seattle
- Université de Washington
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 001797
- to stream Istex, to step Curation: 001797
- to stream Istex, to step Checkpoint: 001019
- to stream PubMed, to step Corpus: 001F31
- to stream PubMed, to step Curation: 001F31
- to stream PubMed, to step Checkpoint: 001F20
- to stream Ncbi, to step Merge: 002433
- to stream Ncbi, to step Curation: 002433
- to stream Ncbi, to step Checkpoint: 002433
- to stream Main, to step Merge: 002C78
- to stream PascalFrancis, to step Corpus: 000F69
- to stream PascalFrancis, to step Curation: 001D50
- to stream PascalFrancis, to step Checkpoint: 000F59
- to stream Main, to step Merge: 003056
- to stream Main, to step Curation: 002417
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">BuChE‐K and APOE ϵ4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline</title><author><name sortKey="Lane, Roger" sort="Lane, Roger" uniqKey="Lane R" first="Roger" last="Lane">Roger Lane</name></author><author><name sortKey="He, Yunsheng" sort="He, Yunsheng" uniqKey="He Y" first="Yunsheng" last="He">Yunsheng He</name></author><author><name sortKey="Morris, Christopher" sort="Morris, Christopher" uniqKey="Morris C" first="Christopher" last="Morris">Christopher Morris</name></author><author><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name></author><author><name sortKey="Emre, Murat" sort="Emre, Murat" uniqKey="Emre M" first="Murat" last="Emre">Murat Emre</name></author><author><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:43734AA6EE8C8464D14EFDDA9F139A3F01EA79FA</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/mds.22357</idno><idno type="url">https://api.istex.fr/document/43734AA6EE8C8464D14EFDDA9F139A3F01EA79FA/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001797</idno><idno type="wicri:Area/Istex/Curation">001797</idno><idno type="wicri:Area/Istex/Checkpoint">001019</idno><idno type="wicri:doubleKey">0885-3185:2009:Lane R:buche:k:and</idno><idno type="wicri:source">PubMed</idno><idno type="RBID">pubmed:19006190</idno><idno type="wicri:Area/PubMed/Corpus">001F31</idno><idno type="wicri:Area/PubMed/Curation">001F31</idno><idno type="wicri:Area/PubMed/Checkpoint">001F20</idno><idno type="wicri:Area/Ncbi/Merge">002433</idno><idno type="wicri:Area/Ncbi/Curation">002433</idno><idno type="wicri:Area/Ncbi/Checkpoint">002433</idno><idno type="wicri:Area/Main/Merge">002C78</idno><idno type="wicri:source">INIST</idno><idno type="RBID">Pascal:09-0136787</idno><idno type="wicri:Area/PascalFrancis/Corpus">000F69</idno><idno type="wicri:Area/PascalFrancis/Curation">001D50</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000F59</idno><idno type="wicri:doubleKey">0885-3185:2009:Lane R:buche:k:and</idno><idno type="wicri:Area/Main/Merge">003056</idno><idno type="wicri:Area/Main/Curation">002417</idno><idno type="wicri:Area/Main/Exploration">002417</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">BuChE‐K and APOE ϵ4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline</title><author><name sortKey="Lane, Roger" sort="Lane, Roger" uniqKey="Lane R" first="Roger" last="Lane">Roger Lane</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Novartis Pharmaceuticals Corporation, East Hanover, New Jersey</wicri:regionArea><placeName><region type="state">New Jersey</region></placeName></affiliation></author><author><name sortKey="He, Yunsheng" sort="He, Yunsheng" uniqKey="He Y" first="Yunsheng" last="He">Yunsheng He</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Clinical Pharmacogenetics, Novartis Pharmaceuticals Corporation, Cambridge, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Morris, Christopher" sort="Morris, Christopher" uniqKey="Morris C" first="Christopher" last="Morris">Christopher Morris</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Newcastle General Hospital, Newcastle upon Tyne</wicri:regionArea><wicri:noRegion>Newcastle upon Tyne</wicri:noRegion></affiliation></author><author><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name><affiliation wicri:level="4"><country xml:lang="fr">États-Unis</country><wicri:regionArea>VA‐Puget Sound Health Care System (MIRECC, PADRECC) and University of Washington, Seattle, Washington</wicri:regionArea><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Emre, Murat" sort="Emre, Murat" uniqKey="Emre M" first="Murat" last="Emre">Murat Emre</name><affiliation wicri:level="1"><country xml:lang="fr">Turquie</country><wicri:regionArea>Istanbul Faculty of Medicine, Istanbul University, Istanbul</wicri:regionArea><wicri:noRegion>Istanbul</wicri:noRegion></affiliation></author><author><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Wolfson Centre for Age Related Diseases, King's College, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-02-15">2009-02-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="392">392</biblScope><biblScope unit="page" to="400">400</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">43734AA6EE8C8464D14EFDDA9F139A3F01EA79FA</idno><idno type="DOI">10.1002/mds.22357</idno><idno type="ArticleID">MDS22357</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Apolipoprotein E</term><term>Apolipoprotein E4 (genetics)</term><term>Butyrylcholinesterase (genetics)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (epidemiology)</term><term>Cognitive disorder</term><term>Female</term><term>Gene Frequency</term><term>Genotype</term><term>Humans</term><term>Hyperhomocysteinemia</term><term>Hyperhomocysteinemia (epidemiology)</term><term>Lewy Body Disease (drug therapy)</term><term>Lewy Body Disease (epidemiology)</term><term>Lewy Body Disease (genetics)</term><term>Lewy body dementia</term><term>Male</term><term>Nervous system diseases</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neuropsychological Tests</term><term>Parkinson disease</term><term>Parkinson's disease dementia</term><term>Phenylcarbamates (therapeutic use)</term><term>Psychomotor Disorders (diagnosis)</term><term>Psychomotor Disorders (epidemiology)</term><term>Randomized Controlled Trials as Topic</term><term>Severity of Illness Index</term><term>apolipoprotein E</term><term>butyrylcholinesterase</term><term>dementia with Lewy bodies</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoprotein E4</term><term>Butyrylcholinesterase</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term><term>Psychomotor Disorders</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lewy Body Disease</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Cognition Disorders</term><term>Hyperhomocysteinemia</term><term>Lewy Body Disease</term><term>Psychomotor Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lewy Body Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term><term>Phenylcarbamates</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Gene Frequency</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term><term>Randomized Controlled Trials as Topic</term><term>Severity of Illness Index</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Apolipoprotéine E</term><term>Démence à corps de Lewy</term><term>Génotype</term><term>Hyperhomocystéinémie</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Trouble cognitif</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apolipoprotein E (APOE) ε4 and butyrylcholinesterase‐K (BuChE‐K) are associated with an increased risk for Alzheimer's disease. The primary objective was to evaluate frequencies of these alleles in dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). A secondary objective was to evaluate influences on rate of cognitive decline. This analysis used data from participants consenting to pharmacogenetic testing in placebo‐controlled rivastigmine studies. Allele frequencies in DLB and PDD were compared using logistic regression. Within the PDD placebo sample, associations with cognitive decline were evaluated (the DLB sample was too small for these evaluations). Fifty‐seven DLB and 323 PDD subjects provided APOE and BuChE data. Allelic frequencies were higher in DLB, relative to PDD subjects, for BuChE‐K (P = 0.06), APOE ε4 (P < 0.001), or both alleles together (P < 0.001). More rapid cognitive decline was seen in PDD patients carrying both alleles, compared with other genotypes. Subjects with hyperhomocysteinemia were associated with more rapid decline in the presence of BuChE‐K, with or without APOE ε4. These results suggest that genetic and biochemical risk factors for AD and PDD pathology may be important in dementia onset and progression in these Lewy body disorders. © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>Turquie</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>Massachusetts</li><li>New Jersey</li><li>Washington (État)</li></region><settlement><li>Londres</li><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><region name="New Jersey"><name sortKey="Lane, Roger" sort="Lane, Roger" uniqKey="Lane R" first="Roger" last="Lane">Roger Lane</name></region><name sortKey="He, Yunsheng" sort="He, Yunsheng" uniqKey="He Y" first="Yunsheng" last="He">Yunsheng He</name><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Morris, Christopher" sort="Morris, Christopher" uniqKey="Morris C" first="Christopher" last="Morris">Christopher Morris</name></noRegion><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name></country><country name="Turquie"><noRegion><name sortKey="Emre, Murat" sort="Emre, Murat" uniqKey="Emre M" first="Murat" last="Emre">Murat Emre</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002417 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002417 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:43734AA6EE8C8464D14EFDDA9F139A3F01EA79FA
|texte= BuChE‐K and APOE ϵ4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline
}}
| This area was generated with Dilib version V0.6.23. |  |