Brain amyloid and cognition in Lewy body diseases.
Identifieur interne : 000D48 ( PubMed/Curation ); précédent : 000D47; suivant : 000D49Brain amyloid and cognition in Lewy body diseases.
Auteurs : Stephen N. Gomperts [États-Unis] ; Joseph J. Locascio ; Marta Marquie ; Andrea L. Santarlasci ; Dorene M. Rentz ; Jacqueline Maye ; Keith A. Johnson ; John H. GrowdonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2012.
English descriptors
- KwdEn :
- Aged, Amyloid beta-Peptides (metabolism), Aniline Compounds (metabolism), Antiparkinson Agents (therapeutic use), Apolipoprotein E3 (genetics), Cognition, Female, Genotype, Humans, Levodopa (therapeutic use), Lewy Body Disease (metabolism), Lewy Body Disease (psychology), Lewy Body Disease (radionuclide imaging), Male, Mild Cognitive Impairment (metabolism), Mild Cognitive Impairment (psychology), Neurologic Examination, Neuropsychological Tests, Parkinson Disease (metabolism), Parkinson Disease (psychology), Positron-Emission Tomography, Thiazoles (metabolism).
- MESH :
- chemical , genetics : Apolipoprotein E3.
- chemical , metabolism : Amyloid beta-Peptides, Aniline Compounds, Thiazoles.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- metabolism : Lewy Body Disease, Mild Cognitive Impairment, Parkinson Disease.
- psychology : Lewy Body Disease, Mild Cognitive Impairment, Parkinson Disease.
- radionuclide imaging : Lewy Body Disease.
- Aged, Cognition, Female, Genotype, Humans, Male, Neurologic Examination, Neuropsychological Tests, Positron-Emission Tomography.
Abstract
Many patients with PD develop PD with dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account, in part, for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases. Twenty-nine cognitively healthy PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD, and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and Pittsburgh compound B (PiB) imaging with PET. Apolipoprotein E (ApoE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference. PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the ApoE ε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition. DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD, or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.
DOI: 10.1002/mds.25048
PubMed: 22693110
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000D48
Links to Exploration step
pubmed:22693110Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Brain amyloid and cognition in Lewy body diseases.</title><author><name sortKey="Gomperts, Stephen N" sort="Gomperts, Stephen N" uniqKey="Gomperts S" first="Stephen N" last="Gomperts">Stephen N. Gomperts</name><affiliation wicri:level="1"><nlm:affiliation>Massachusetts General Hospital, 15 Parkman Street, Boston, MA 02114,USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Massachusetts General Hospital, 15 Parkman Street, Boston, MA 02114</wicri:regionArea></affiliation></author><author><name sortKey="Locascio, Joseph J" sort="Locascio, Joseph J" uniqKey="Locascio J" first="Joseph J" last="Locascio">Joseph J. Locascio</name></author><author><name sortKey="Marquie, Marta" sort="Marquie, Marta" uniqKey="Marquie M" first="Marta" last="Marquie">Marta Marquie</name></author><author><name sortKey="Santarlasci, Andrea L" sort="Santarlasci, Andrea L" uniqKey="Santarlasci A" first="Andrea L" last="Santarlasci">Andrea L. Santarlasci</name></author><author><name sortKey="Rentz, Dorene M" sort="Rentz, Dorene M" uniqKey="Rentz D" first="Dorene M" last="Rentz">Dorene M. Rentz</name></author><author><name sortKey="Maye, Jacqueline" sort="Maye, Jacqueline" uniqKey="Maye J" first="Jacqueline" last="Maye">Jacqueline Maye</name></author><author><name sortKey="Johnson, Keith A" sort="Johnson, Keith A" uniqKey="Johnson K" first="Keith A" last="Johnson">Keith A. Johnson</name></author><author><name sortKey="Growdon, John H" sort="Growdon, John H" uniqKey="Growdon J" first="John H" last="Growdon">John H. Growdon</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="doi">10.1002/mds.25048</idno><idno type="RBID">pubmed:22693110</idno><idno type="pmid">22693110</idno><idno type="wicri:Area/PubMed/Corpus">000D48</idno><idno type="wicri:Area/PubMed/Curation">000D48</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Brain amyloid and cognition in Lewy body diseases.</title><author><name sortKey="Gomperts, Stephen N" sort="Gomperts, Stephen N" uniqKey="Gomperts S" first="Stephen N" last="Gomperts">Stephen N. Gomperts</name><affiliation wicri:level="1"><nlm:affiliation>Massachusetts General Hospital, 15 Parkman Street, Boston, MA 02114,USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Massachusetts General Hospital, 15 Parkman Street, Boston, MA 02114</wicri:regionArea></affiliation></author><author><name sortKey="Locascio, Joseph J" sort="Locascio, Joseph J" uniqKey="Locascio J" first="Joseph J" last="Locascio">Joseph J. Locascio</name></author><author><name sortKey="Marquie, Marta" sort="Marquie, Marta" uniqKey="Marquie M" first="Marta" last="Marquie">Marta Marquie</name></author><author><name sortKey="Santarlasci, Andrea L" sort="Santarlasci, Andrea L" uniqKey="Santarlasci A" first="Andrea L" last="Santarlasci">Andrea L. Santarlasci</name></author><author><name sortKey="Rentz, Dorene M" sort="Rentz, Dorene M" uniqKey="Rentz D" first="Dorene M" last="Rentz">Dorene M. Rentz</name></author><author><name sortKey="Maye, Jacqueline" sort="Maye, Jacqueline" uniqKey="Maye J" first="Jacqueline" last="Maye">Jacqueline Maye</name></author><author><name sortKey="Johnson, Keith A" sort="Johnson, Keith A" uniqKey="Johnson K" first="Keith A" last="Johnson">Keith A. Johnson</name></author><author><name sortKey="Growdon, John H" sort="Growdon, John H" uniqKey="Growdon J" first="John H" last="Growdon">John H. Growdon</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="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Amyloid beta-Peptides (metabolism)</term><term>Aniline Compounds (metabolism)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Apolipoprotein E3 (genetics)</term><term>Cognition</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Lewy Body Disease (metabolism)</term><term>Lewy Body Disease (psychology)</term><term>Lewy Body Disease (radionuclide imaging)</term><term>Male</term><term>Mild Cognitive Impairment (metabolism)</term><term>Mild Cognitive Impairment (psychology)</term><term>Neurologic Examination</term><term>Neuropsychological Tests</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (psychology)</term><term>Positron-Emission Tomography</term><term>Thiazoles (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoprotein E3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Aniline Compounds</term><term>Thiazoles</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lewy Body Disease</term><term>Mild Cognitive Impairment</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Lewy Body Disease</term><term>Mild Cognitive Impairment</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Lewy Body Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cognition</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Neurologic Examination</term><term>Neuropsychological Tests</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Many patients with PD develop PD with dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account, in part, for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases. Twenty-nine cognitively healthy PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD, and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and Pittsburgh compound B (PiB) imaging with PET. Apolipoprotein E (ApoE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference. PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the ApoE ε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition. DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD, or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">22693110</PMID><DateCreated><Year>2012</Year><Month>07</Month><Day>18</Day></DateCreated><DateCompleted><Year>2012</Year><Month>11</Month><Day>21</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>8</Issue><PubDate><Year>2012</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Brain amyloid and cognition in Lewy body diseases.</ArticleTitle><Pagination><MedlinePgn>965-73</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25048</ELocationID><Abstract><AbstractText>Many patients with PD develop PD with dementia (PDD), a syndrome that overlaps clinically and pathologically with dementia with Lewy bodies (DLB); PDD and DLB differ chiefly in the relative timing of dementia and parkinsonism. Brain amyloid deposition is an early feature of DLB and may account, in part, for its early dementia. We sought to confirm this hypothesis and also to determine whether amyloid accumulation contributes to cognitive impairment and dementia in the broad range of parkinsonian diseases. Twenty-nine cognitively healthy PD, 14 PD subjects with mild cognitive impairment (PD-MCI), 18 with DLB, 12 with PDD, and 85 healthy control subjects (HCS) underwent standardized neurologic and neuropsychological examinations and Pittsburgh compound B (PiB) imaging with PET. Apolipoprotein E (ApoE) genotypes were obtained in many patients. PiB retention was expressed as the distribution volume ratio using a cerebellar tissue reference. PiB retention was significantly higher in DLB than in any of the other diagnostic groups. PiB retention did not differ across PDD, PD-MCI, PD, and HCS. Amyloid burden increased with age and with the presence of the ApoE ε4 allele in all patient groups. Only in the DLB group was amyloid deposition associated with impaired cognition. DLB subjects have higher amyloid burden than subjects with PDD, PD-MCI, PD, or HCS; amyloid deposits are linked to cognitive impairment only in DLB. Early amyloid deposits in DLB relative to PDD may account for their difference in the timing of dementia and parkinsonism.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gomperts</LastName><ForeName>Stephen N</ForeName><Initials>SN</Initials><AffiliationInfo><Affiliation>Massachusetts General Hospital, 15 Parkman Street, Boston, MA 02114,USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Locascio</LastName><ForeName>Joseph J</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Marquie</LastName><ForeName>Marta</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Santarlasci</LastName><ForeName>Andrea L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Rentz</LastName><ForeName>Dorene M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Maye</LastName><ForeName>Jacqueline</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Johnson</LastName><ForeName>Keith A</ForeName><Initials>KA</Initials></Author><Author ValidYN="Y"><LastName>Growdon</LastName><ForeName>John H</ForeName><Initials>JH</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>5 U01 AG016976-11</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AG036694</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 AG005134</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 AG016976</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>06</Month><Day>12</Day></ArticleDate></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="C475519">2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000814">Aniline Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053318">Apolipoprotein E3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013844">Thiazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Brain. 2008 Jun;131(Pt 6):1630-45</RefSource><PMID Version="1">18339640</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2008 Sep 16;71(12):903-10</RefSource><PMID Version="1">18794492</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 2012 May;33(5):878-85</RefSource><PMID Version="1">20961664</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 2008 Dec;79(12):1331-8</RefSource><PMID Version="1">18653550</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2008 Dec 19;448(1):20-3</RefSource><PMID Version="1">18930114</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neuropathol. 1998 Jun;95(6):576-82</RefSource><PMID Version="1">9650749</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2005 Nov 16;25(46):10598-606</RefSource><PMID Version="1">16291932</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Nucl Med. 2005 Dec;46(12):1959-72</RefSource><PMID Version="1">16330558</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2005 Dec 27;65(12):1863-72</RefSource><PMID Version="1">16237129</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2006 Jan;21(1):45-9</RefSource><PMID Version="1">16116614</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2006 Mar;59(3):512-9</RefSource><PMID Version="1">16372280</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2006 Jul;60(1):145-7</RefSource><PMID Version="1">16802294</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2006 Aug 8;67(3):446-52</RefSource><PMID Version="1">16894106</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2007 Feb;64(2):261-5</RefSource><PMID Version="1">17296843</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2007 Mar 6;414(2):141-4</RefSource><PMID Version="1">17204369</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2007 May 15;68(20):1718-25</RefSource><PMID Version="1">17502554</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2007 Sep;62(3):229-34</RefSource><PMID Version="1">17683091</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2007 Sep 15;22(12):1689-707; quiz 1837</RefSource><PMID Version="1">17542011</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurologia. 2008 Apr;23(3):152-6</RefSource><PMID Version="1">18370334</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2009;24 Suppl 2:S742-7</RefSource><PMID Version="1">19877240</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2010 Jan 5;74(1):77-84</RefSource><PMID Version="1">20038776</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2010 Jan;67(1):122-31</RefSource><PMID Version="1">20186853</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2010 Jun;133(Pt 6):1755-62</RefSource><PMID Version="1">20371510</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2010 Nov 15;25(15):2516-23</RefSource><PMID Version="1">20922808</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2011 Mar;17(3):160-5</RefSource><PMID Version="1">21195652</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lancet Neurol. 2011 Mar;10(3):241-52</RefSource><PMID Version="1">21349439</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2011 Jun;69(6):1032-42</RefSource><PMID Version="1">21437929</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2011 Aug 15;26(10):1814-24</RefSource><PMID Version="1">21661055</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm. 2012 Mar;119(3):381-2</RefSource><PMID Version="1">21960008</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2000 Jan 25;54(2):407-11</RefSource><PMID Version="1">10668703</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2000 Feb 22;54(4):827-32</RefSource><PMID Version="1">10690971</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2000 Apr 25;54(8):1596-602</RefSource><PMID Version="1">10762499</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neuropathol. 2001 Oct;102(4):355-63</RefSource><PMID Version="1">11603811</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Geriatr Psychiatry Neurol. 2002 Winter;15(4):210-6</RefSource><PMID Version="1">12489917</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 2003 Mar-Apr;24(2):197-211</RefSource><PMID Version="1">12498954</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Exp Neuropsychol. 2003 Feb;25(1):94-109</RefSource><PMID Version="1">12607175</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2003 Mar;60(3):387-92</RefSource><PMID Version="1">12633150</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Alzheimers Dis. 2003 Apr;5(2):119-25</RefSource><PMID Version="1">12719629</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Med Chem. 2003 Jun 19;46(13):2740-54</RefSource><PMID Version="1">12801237</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Sci. 2003 Dec 15;216(1):105-8</RefSource><PMID Version="1">14607310</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2004 Jan 27;62(2):181-7</RefSource><PMID Version="1">14745051</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Wiad Lek. 2004;57(1-2):20-4</RefSource><PMID Version="1">15181744</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2004 Jun 22;62(12):2198-202</RefSource><PMID Version="1">15210882</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1967 May;17(5):427-42</RefSource><PMID Version="1">6067254</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Psychiatr Res. 1975 Nov;12(3):189-98</RefSource><PMID Version="1">1202204</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1982 Feb;32(2):133-7</RefSource><PMID Version="1">7198740</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Br J Psychiatry. 1982 Jun;140:566-72</RefSource><PMID Version="1">7104545</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1988 May;45(5):497-501</RefSource><PMID Version="1">3358699</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1989 Jul;26(1):47-50</RefSource><PMID Version="1">2549846</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1990 Oct;40(10):1513-7</RefSource><PMID Version="1">2215941</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1992 Dec;49(12):1253-8</RefSource><PMID Version="1">1449404</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1993 Feb;50(2):140-8</RefSource><PMID Version="1">8431132</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1993 Aug 13;261(5123):921-3</RefSource><PMID Version="1">8346443</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1993 Nov;43(11):2412-4</RefSource><PMID Version="1">8232972</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1994 Dec;44(12):2308-14</RefSource><PMID Version="1">7991117</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 1994 Dec;145(6):1472-84</RefSource><PMID Version="1">7992850</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 1994 Nov 21;182(1):1-2</RefSource><PMID Version="1">7891871</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cereb Blood Flow Metab. 1996 Sep;16(5):834-40</RefSource><PMID Version="1">8784228</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm Suppl. 1996;47:205-18</RefSource><PMID Version="1">8841967</PMID></CommentsCorrections><CommentsCorrections RefType="CommentIn"><RefSource>Mov Disord. 2013 Mar;28(3):406</RefSource><PMID Version="1">23390062</PMID></CommentsCorrections><CommentsCorrections RefType="CommentIn"><RefSource>Mov Disord. 2013 Mar;28(3):407</RefSource><PMID Version="1">23401107</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016229">Amyloid beta-Peptides</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000814">Aniline Compounds</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D053318">Apolipoprotein E3</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D003071">Cognition</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005838">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020961">Lewy Body Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000523">psychology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D060825">Mild Cognitive Impairment</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000523">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009483">Neuropsychological Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000523">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D049268">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013844">Thiazoles</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS373304</OtherID><OtherID Source="NLM">PMC3725259</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>2</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>3</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>4</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2012</Year><Month>6</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>6</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>6</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.25048</ArticleId><ArticleId IdType="pubmed">22693110</ArticleId><ArticleId IdType="pmc">PMC3725259</ArticleId><ArticleId IdType="mid">NIHMS373304</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D48 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000D48 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:22693110
|texte= Brain amyloid and cognition in Lewy body diseases.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:22693110" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a MovDisordV3
| This area was generated with Dilib version V0.6.23. |  |