Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease
Identifieur interne : 001C20 ( Istex/Corpus ); précédent : 001C19; suivant : 001C21Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease
Auteurs : G A Marshall ; D I Kaufer ; O L Lopez ; G R Rao ; R L Hamilton ; S T DekoskySource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2004-10.
English descriptors
- KwdEn :
- 2aware, 2aware subjects, Alzheimer’s disease, Anosognosia, Anterior cingulate cortex, Arch neurol, Aware subjects, Brain regions, Chapel hill, Cholinergic, Clinical data, Clinicopathological correlation studies, Cognitive, Cognitive deficits, Current study, Deficit awareness, Dementia, Dementia severity, Different brain regions, Disease subjects, Entorhinal, Entorhinal cortex, Feedback projections, Frontal lobe dysfunction, Future studies, Hippocampal formation, Hippocampus, Kaufer, Last examination, Medical center, Mmse score, Multiple comparisons, National institute, Neural networks, Neurofibrillary tangle, Neurol, Neurol neurosurg psychiatry, Neuropathological, Neuropathological data, Neuropsychiatry clin neurosci, Other regions, Pathological correlates, Pathological substrates, Plaque, Prosubiculum, Putative role, Right hemisphere, Right prosubiculum region, Senile plaque, Senile plaque counts, Several studies, State examination scores, Subset analysis, Temporal regions, acetylcholine, anosognosia.
- Teeft :
- 2aware, 2aware subjects, Anosognosia, Anterior cingulate cortex, Arch neurol, Aware subjects, Brain regions, Chapel hill, Cholinergic, Clinical data, Clinicopathological correlation studies, Cognitive, Cognitive deficits, Current study, Deficit awareness, Dementia, Dementia severity, Different brain regions, Disease subjects, Entorhinal, Entorhinal cortex, Feedback projections, Frontal lobe dysfunction, Future studies, Hippocampal formation, Hippocampus, Kaufer, Last examination, Medical center, Mmse score, Multiple comparisons, National institute, Neural networks, Neurofibrillary tangle, Neurol, Neurol neurosurg psychiatry, Neuropathological, Neuropathological data, Neuropsychiatry clin neurosci, Other regions, Pathological correlates, Pathological substrates, Plaque, Prosubiculum, Putative role, Right hemisphere, Right prosubiculum region, Senile plaque, Senile plaque counts, Several studies, State examination scores, Subset analysis, Temporal regions.
Abstract
Background: Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions. Objective: To investigate pathological correlates of anosognosia in Alzheimer’s disease. Design: 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC). Results: SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002). Conclusions: Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.
Url:
DOI: 10.1136/jnnp.2003.030007
Links to Exploration step
ISTEX:796FADF533B7FEAEA13E1DE89BB3AF0C3114118DLe document en format XML
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R L" uniqKey="Hamilton R" first="R L" last="Hamilton">R L Hamilton</name><affiliation><mods:affiliation>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</mods:affiliation></affiliation></author><author><name sortKey="Dekosky, S T" sort="Dekosky, S T" uniqKey="Dekosky S" first="S T" last="Dekosky">S T Dekosky</name><affiliation><mods:affiliation>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2004-10">2004-10</date><biblScope unit="volume">75</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1396">1396</biblScope></imprint><idno type="ISSN">0022-3050</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2aware</term><term>2aware subjects</term><term>Alzheimer’s disease</term><term>Anosognosia</term><term>Anterior cingulate cortex</term><term>Arch neurol</term><term>Aware subjects</term><term>Brain regions</term><term>Chapel hill</term><term>Cholinergic</term><term>Clinical data</term><term>Clinicopathological correlation studies</term><term>Cognitive</term><term>Cognitive deficits</term><term>Current study</term><term>Deficit awareness</term><term>Dementia</term><term>Dementia severity</term><term>Different brain regions</term><term>Disease subjects</term><term>Entorhinal</term><term>Entorhinal cortex</term><term>Feedback projections</term><term>Frontal lobe dysfunction</term><term>Future studies</term><term>Hippocampal formation</term><term>Hippocampus</term><term>Kaufer</term><term>Last examination</term><term>Medical center</term><term>Mmse score</term><term>Multiple comparisons</term><term>National institute</term><term>Neural networks</term><term>Neurofibrillary tangle</term><term>Neurol</term><term>Neurol neurosurg psychiatry</term><term>Neuropathological</term><term>Neuropathological data</term><term>Neuropsychiatry clin neurosci</term><term>Other regions</term><term>Pathological correlates</term><term>Pathological substrates</term><term>Plaque</term><term>Prosubiculum</term><term>Putative role</term><term>Right hemisphere</term><term>Right prosubiculum region</term><term>Senile plaque</term><term>Senile plaque counts</term><term>Several studies</term><term>State examination scores</term><term>Subset analysis</term><term>Temporal regions</term><term>acetylcholine</term><term>anosognosia</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>2aware</term><term>2aware subjects</term><term>Anosognosia</term><term>Anterior cingulate cortex</term><term>Arch neurol</term><term>Aware subjects</term><term>Brain regions</term><term>Chapel hill</term><term>Cholinergic</term><term>Clinical data</term><term>Clinicopathological correlation studies</term><term>Cognitive</term><term>Cognitive deficits</term><term>Current study</term><term>Deficit awareness</term><term>Dementia</term><term>Dementia severity</term><term>Different brain regions</term><term>Disease subjects</term><term>Entorhinal</term><term>Entorhinal cortex</term><term>Feedback projections</term><term>Frontal lobe dysfunction</term><term>Future studies</term><term>Hippocampal formation</term><term>Hippocampus</term><term>Kaufer</term><term>Last examination</term><term>Medical center</term><term>Mmse score</term><term>Multiple comparisons</term><term>National institute</term><term>Neural networks</term><term>Neurofibrillary tangle</term><term>Neurol</term><term>Neurol neurosurg psychiatry</term><term>Neuropathological</term><term>Neuropathological data</term><term>Neuropsychiatry clin neurosci</term><term>Other regions</term><term>Pathological correlates</term><term>Pathological substrates</term><term>Plaque</term><term>Prosubiculum</term><term>Putative role</term><term>Right hemisphere</term><term>Right prosubiculum region</term><term>Senile plaque</term><term>Senile plaque counts</term><term>Several studies</term><term>State examination scores</term><term>Subset analysis</term><term>Temporal regions</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions. Objective: To investigate pathological correlates of anosognosia in Alzheimer’s disease. Design: 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC). Results: SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002). Conclusions: Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.</div></front></TEI><istex><corpusName>bmj</corpusName><keywords><teeft><json:string>anosognosia</json:string><json:string>2aware</json:string><json:string>prosubiculum</json:string><json:string>dementia</json:string><json:string>neuropathological</json:string><json:string>entorhinal</json:string><json:string>2aware subjects</json:string><json:string>entorhinal cortex</json:string><json:string>neurol</json:string><json:string>dementia severity</json:string><json:string>cholinergic</json:string><json:string>hippocampus</json:string><json:string>kaufer</json:string><json:string>cognitive deficits</json:string><json:string>hippocampal formation</json:string><json:string>arch neurol</json:string><json:string>senile plaque</json:string><json:string>aware subjects</json:string><json:string>plaque</json:string><json:string>other regions</json:string><json:string>temporal regions</json:string><json:string>current study</json:string><json:string>neurofibrillary tangle</json:string><json:string>clinical data</json:string><json:string>brain regions</json:string><json:string>neurol neurosurg psychiatry</json:string><json:string>subset analysis</json:string><json:string>future studies</json:string><json:string>medical center</json:string><json:string>pathological correlates</json:string><json:string>state examination scores</json:string><json:string>anterior cingulate cortex</json:string><json:string>neuropathological data</json:string><json:string>chapel hill</json:string><json:string>last examination</json:string><json:string>mmse score</json:string><json:string>senile plaque counts</json:string><json:string>different brain regions</json:string><json:string>pathological substrates</json:string><json:string>multiple comparisons</json:string><json:string>right prosubiculum region</json:string><json:string>putative role</json:string><json:string>feedback projections</json:string><json:string>right hemisphere</json:string><json:string>deficit awareness</json:string><json:string>clinicopathological correlation studies</json:string><json:string>neural networks</json:string><json:string>disease subjects</json:string><json:string>national institute</json:string><json:string>frontal lobe dysfunction</json:string><json:string>neuropsychiatry clin neurosci</json:string><json:string>several studies</json:string><json:string>cognitive</json:string></teeft></keywords><author><json:item><name>G A Marshall</name><affiliations><json:string>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>D I Kaufer</name><affiliations><json:string>Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA</json:string></affiliations></json:item><json:item><name>O L Lopez</name><affiliations><json:string>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</json:string></affiliations></json:item><json:item><name>G R Rao</name><affiliations><json:string>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</json:string></affiliations></json:item><json:item><name>R L Hamilton</name><affiliations><json:string>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</json:string></affiliations></json:item><json:item><name>S T DeKosky</name><affiliations><json:string>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</json:string><json:string>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer’s disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>anosognosia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>acetylcholine</value></json:item></subject><arkIstex>ark:/67375/NVC-VGGRB72M-8</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Background: Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions. Objective: To investigate pathological correlates of anosognosia in Alzheimer’s disease. Design: 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC). Results: SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002). Conclusions: Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.</abstract><qualityIndicators><score>8.373</score><pdfWordCount>3373</pdfWordCount><pdfCharCount>23264</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>255</abstractWordCount><abstractCharCount>1828</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</title><pmid><json:string>15377684</json:string></pmid><genre><json:string>research-article</json:string></genre><host><title>Journal of Neurology, Neurosurgery & Psychiatry</title><language><json:string>unknown</json:string></language><issn><json:string>0022-3050</json:string></issn><eissn><json:string>1468-330X</json:string></eissn><volume>75</volume><issue>10</issue><pages><first>1396</first></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Memory disorders (neurology)</value></json:item><json:item><value>Memory disorders (psychiatry)</value></json:item></subject></host><namedEntities><unitex><date><json:string>2004-09-16</json:string><json:string>6200</json:string></date><geogName></geogName><orgName><json:string>Chad Karoleski</json:string><json:string>University of Pittsburgh Alzheimer</json:string><json:string>US National Institute on Aging Center</json:string><json:string>Department of Pathology</json:string><json:string>University of Pittsburgh</json:string><json:string>Department of Neurology, University of Pittsburgh and Pittsburgh</json:string><json:string>Disease Research Center</json:string><json:string>VA Medical Center, Pittsburgh</json:string><json:string>ADRC</json:string><json:string>Disease Research Center, University of Pittsburgh and Pittsburgh</json:string><json:string>Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA Competing</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Ott</json:string><json:string>Hyman</json:string><json:string>Gutti</json:string><json:string>John Moossy</json:string><json:string>Julio Martinez</json:string><json:string>R. Rao</json:string><json:string>Santillan</json:string></persName><placeName></placeName><ref_url></ref_url><ref_bibl><json:string>Michon et al</json:string><json:string>Ott et al</json:string><json:string>Lopez et al</json:string><json:string>Reed et al</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/NVC-VGGRB72M-8</json:string></ark><categories><wos><json:string>1 - social science</json:string><json:string>2 - psychiatry</json:string><json:string>1 - science</json:string><json:string>2 - surgery</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - neurology & neurosurgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Psychiatry and Mental health</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Surgery</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - neurologie</json:string></inist></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1136/jnnp.2003.030007</json:string></doi><id>796FADF533B7FEAEA13E1DE89BB3AF0C3114118D</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://publisher-list.data.istex.fr">BMJ Publishing Group Ltd</publisher><availability><licence><p>Copyright 2004 Journal of Neurology Neurosurgery and Psychiatry</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-7M42M2QJ-2">bmj</p></availability><date>2004-09-16</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>Correspondence to:
Dr D Kaufer
UNC School of Medicine, CB# 7025, 3114 Bioinformatics Bldg, Chapel Hill, NC 27599, USA; kauferd@glial.med.unc.edu</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</title><author xml:id="author-0000"><persName><forename type="first">G A</forename><surname>Marshall</surname></persName><affiliation>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">D I</forename><surname>Kaufer</surname></persName><affiliation>Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">O L</forename><surname>Lopez</surname></persName><affiliation>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</affiliation></author><author xml:id="author-0003"><persName><forename type="first">G R</forename><surname>Rao</surname></persName><affiliation>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</affiliation></author><author xml:id="author-0004"><persName><forename type="first">R L</forename><surname>Hamilton</surname></persName><affiliation>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</affiliation></author><author xml:id="author-0005"><persName><forename type="first">S T</forename><surname>DeKosky</surname></persName><affiliation>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</affiliation><affiliation>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</affiliation></author><idno type="istex">796FADF533B7FEAEA13E1DE89BB3AF0C3114118D</idno><idno type="ark">ark:/67375/NVC-VGGRB72M-8</idno><idno type="DOI">10.1136/jnnp.2003.030007</idno><idno type="href">jnnp-75-1396.pdf</idno><idno type="PMID">15377684</idno><idno type="local">0751396</idno></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><idno type="PublisherID-hwp">jnnp</idno><idno type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2004-10"></date><biblScope unit="volume">75</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1396">1396</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004-09-16</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background: Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions. Objective: To investigate pathological correlates of anosognosia in Alzheimer’s disease. Design: 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC). Results: SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002). Conclusions: Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Alzheimer’s disease</term></item><item><term>anosognosia</term></item><item><term>acetylcholine</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>hwp-journal-coll</head><item><term>Memory disorders (neurology)</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>hwp-journal-coll</head><item><term>Memory disorders (psychiatry)</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-09-16">Created</change><change when="2004-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">0751396</article-id><article-id pub-id-type="doi">10.1136/jnnp.2003.030007</article-id><article-id pub-id-type="other">jnnp;75/10/1396</article-id><article-id pub-id-type="pmid">15377684</article-id><article-id pub-id-type="other">1396</article-id><article-id pub-id-type="other">jnnp.2003.030007</article-id><article-categories><subj-group subj-group-type="heading"><subject content-type="original">Papers</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Memory disorders (neurology)</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Memory disorders (psychiatry)</subject></subj-group></article-categories><title-group><article-title>Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Marshall</surname><given-names>G A</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Kaufer</surname><given-names>D I</given-names></name><xref rid="AFF4">4</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Lopez</surname><given-names>O L</given-names></name><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Rao</surname><given-names>G R</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hamilton</surname><given-names>R L</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>DeKosky</surname><given-names>S T</given-names></name><xref rid="AFF1">1</xref><xref rid="AFF3">3</xref></contrib><aff id="AFF1"><label>1</label>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</aff><aff id="AFF2"><label>2</label>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</aff><aff id="AFF3"><label>3</label>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</aff><aff id="AFF4"><label>4</label>Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA</aff></contrib-group><author-notes><corresp>Correspondence to:
Dr D Kaufer
UNC School of Medicine, CB# 7025, 3114 Bioinformatics Bldg, Chapel Hill, NC 27599, USA; <ext-link xlink:href="kauferdglial.med.unc.edu" ext-link-type="email" xlink:type="simple">kauferd@glial.med.unc.edu</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>10</month><year>2004</year></pub-date><pub-date pub-type="epub"><day>16</day><month>9</month><year>2004</year></pub-date><volume>75</volume><volume-id pub-id-type="other">75</volume-id><volume-id pub-id-type="other">75</volume-id><issue>10</issue><issue-id pub-id-type="other">jnnp;75/10</issue-id><issue-id pub-id-type="other">10</issue-id><issue-id pub-id-type="other">75/10</issue-id><fpage>1396</fpage><history><date date-type="accepted"><day>20</day><month>12</month><year>2003</year></date><date date-type="received"><day>08</day><month>10</month><year>2003</year></date><date date-type="rev-recd"><day>19</day><month>12</month><year>2003</year></date></history><permissions><copyright-statement>Copyright 2004 Journal of Neurology Neurosurgery and Psychiatry</copyright-statement><copyright-year>2004</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-75-1396.pdf"></self-uri><abstract xml:lang="en"><p><bold>Background:</bold> Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions.</p><p><bold>Objective:</bold> To investigate pathological correlates of anosognosia in Alzheimer’s disease.</p><p><bold>Design:</bold> 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC).</p><p><bold>Results:</bold> SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002).</p><p><bold>Conclusions:</bold> Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Alzheimer’s disease</kwd><kwd>anosognosia</kwd><kwd>acetylcholine</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Right prosubiculum amyloid plaque density correlates with anosognosia in Alzheimer’s disease</title></titleInfo><name type="personal"><namePart type="given">G A</namePart><namePart type="family">Marshall</namePart><affiliation>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D I</namePart><namePart type="family">Kaufer</namePart><affiliation>Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O L</namePart><namePart type="family">Lopez</namePart><affiliation>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G R</namePart><namePart type="family">Rao</namePart><affiliation>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R L</namePart><namePart type="family">Hamilton</namePart><affiliation>Department of Pathology (Neuropathology), University of Pittsburgh and Pittsburgh VA Medical Center</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S T</namePart><namePart type="family">DeKosky</namePart><affiliation>Department of Neurology, University of Pittsburgh and Pittsburgh VA Medical Center, Pittsburgh, Pennsylvania, USA</affiliation><affiliation>Alzheimer’s Disease Research Center, University of Pittsburgh and Pittsburgh VA Medical Center</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2004-10</dateIssued><dateCreated encoding="w3cdtf">2004-09-16</dateCreated><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Background: Anosognosia is a common manifestation of Alzheimer’s disease. There is an association between impaired awareness and frontal-executive cognitive deficits. Anosognosia is also correlated with decreased metabolism in the right hemisphere, particularly in frontal lobe regions. Objective: To investigate pathological correlates of anosognosia in Alzheimer’s disease. Design: 41 subjects followed longitudinally in the University of Pittsburgh memory disorders clinic and with necropsy verified Alzheimer’s disease were divided into two groups, based on previous clinical assessment: +Aware (n = 23) and −Aware (n = 18). A subset analysis matching subjects for dementia severity using mini-mental state examination scores was also carried out (13 +Aware; 13 −Aware). Histopathological data from necropsy brain tissue consisted of senile plaque (SP) and neurofibrillary tangle (NFT) counts (regional density) from four different brain regions in the right and left hemispheres: superior and middle frontal gyri (SMF), superior temporal isocortex (ST), the prosubiculum of the hippocampus (PRO), and the entorhinal cortex (EC). Results: SP density was greater in the right PRO region of −Aware subjects (F = 6.54, p = 0.015) than +Aware subjects. Significant differences between SP or NFT density were not observed in any other regions. In the subset analysis matching for dementia severity, SP density was again greater in the right PRO region of −Aware subjects than in the other regions (F = 12.72, p = 0.002). Conclusions: Increased SP density in the right PRO region suggests that selective pathological involvement of this area contributes to awareness deficits in Alzheimer’s disease. The putative role of the PRO in self appraisal may reflect its interconnections with other medial temporal and prefrontal regions.</abstract><note type="author-notes">Correspondence to:
Dr D Kaufer
UNC School of Medicine, CB# 7025, 3114 Bioinformatics Bldg, Chapel Hill, NC 27599, USA; kauferd@glial.med.unc.edu</note><subject lang="en"><genre>KWD</genre><topic>Alzheimer’s disease</topic><topic>anosognosia</topic><topic>acetylcholine</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>hwp-journal-coll</genre><topic>Memory disorders (neurology)</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Memory disorders (psychiatry)</topic></subject><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>75</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1396</start></extent></part></relatedItem><identifier type="istex">796FADF533B7FEAEA13E1DE89BB3AF0C3114118D</identifier><identifier type="ark">ark:/67375/NVC-VGGRB72M-8</identifier><identifier type="DOI">10.1136/jnnp.2003.030007</identifier><identifier type="href">jnnp-75-1396.pdf</identifier><identifier type="PMID">15377684</identifier><identifier type="local">0751396</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright 2004 Journal of Neurology Neurosurgery and Psychiatry</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-7M42M2QJ-2">bmj</recordContentSource><recordOrigin>Copyright 2004 Journal of Neurology Neurosurgery and Psychiatry</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/metadata/json</uri></json:item></metadata><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/796FADF533B7FEAEA13E1DE89BB3AF0C3114118D/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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