BuChE-K and APOE epsilon4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline.
Identifieur interne : 001F31 ( PubMed/Corpus ); précédent : 001F30; suivant : 001F32BuChE-K and APOE epsilon4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline.
Auteurs : Roger Lane ; Yunsheng He ; Christopher Morris ; James B. Leverenz ; Murat Emre ; Clive BallardSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Aged, Apolipoprotein E4 (genetics), Butyrylcholinesterase (genetics), Cognition Disorders (diagnosis), Cognition Disorders (epidemiology), Female, Gene Frequency, Genotype, Humans, Hyperhomocysteinemia (epidemiology), Lewy Body Disease (drug therapy), Lewy Body Disease (epidemiology), Lewy Body Disease (genetics), Male, Neuroprotective Agents (therapeutic use), Neuropsychological Tests, Phenylcarbamates (therapeutic use), Psychomotor Disorders (diagnosis), Psychomotor Disorders (epidemiology), Randomized Controlled Trials as Topic, Severity of Illness Index.
- 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) epsilon4 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 epsilon4 (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 epsilon4. 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.
DOI: 10.1002/mds.22357
PubMed: 19006190
Links to Exploration step
pubmed:19006190Le document en format XML
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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">PubMed</idno><date when="2009">2009</date><idno type="doi">10.1002/mds.22357</idno><idno type="RBID">pubmed:19006190</idno><idno type="pmid">19006190</idno><idno type="wicri:Area/PubMed/Corpus">001F31</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">BuChE-K and APOE epsilon4 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><nlm:affiliation>Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936-1080, USA. roger.lane@novartis.com</nlm:affiliation></affiliation></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></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Apolipoprotein E4 (genetics)</term><term>Butyrylcholinesterase (genetics)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (epidemiology)</term><term>Female</term><term>Gene Frequency</term><term>Genotype</term><term>Humans</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>Male</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neuropsychological Tests</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></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></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apolipoprotein E (APOE) epsilon4 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 epsilon4 (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 epsilon4. 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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19006190</PMID><DateCreated><Year>2009</Year><Month>03</Month><Day>03</Day></DateCreated><DateCompleted><Year>2009</Year><Month>07</Month><Day>27</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>3</Issue><PubDate><Year>2009</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>BuChE-K and APOE epsilon4 allele frequencies in Lewy body dementias, and influence of genotype and hyperhomocysteinemia on cognitive decline.</ArticleTitle><Pagination><MedlinePgn>392-400</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22357</ELocationID><Abstract><AbstractText>Apolipoprotein E (APOE) epsilon4 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 epsilon4 (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 epsilon4. 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.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lane</LastName><ForeName>Roger</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936-1080, USA. roger.lane@novartis.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Yunsheng</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Morris</LastName><ForeName>Christopher</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Leverenz</LastName><ForeName>James B</ForeName><Initials>JB</Initials></Author><Author ValidYN="Y"><LastName>Emre</LastName><ForeName>Murat</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Ballard</LastName><ForeName>Clive</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G0400074</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G0502157</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>P50 AG005136</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 AG005136-25</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053327">Apolipoprotein E4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048448">Phenylcarbamates</NameOfSubstance></Chemical><Chemical><RegistryNumber>123441-03-2</RegistryNumber><NameOfSubstance UI="C072506">rivastigmine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.-</RegistryNumber><NameOfSubstance UI="D002091">Butyrylcholinesterase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D053327">Apolipoprotein 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UI="D020138">Hyperhomocysteinemia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020961">Lewy Body Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018696">Neuroprotective Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009483">Neuropsychological Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D048448">Phenylcarbamates</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011596">Psychomotor Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000453">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016032">Randomized Controlled Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012720">Severity of Illness Index</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>11</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>7</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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