Frontotemporal lobar degeneration and dementia with Lewy bodies: Clinicopathological issues associated with antemortem diagnosis
Identifieur interne : 001B62 ( Main/Corpus ); précédent : 001B61; suivant : 001B63Frontotemporal lobar degeneration and dementia with Lewy bodies: Clinicopathological issues associated with antemortem diagnosis
Auteurs : Osamu YokotaSource :
- Psychogeriatrics [ 1346-3500 ] ; 2009-06.
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Abstract
Currently, the clinical diagnostic criteria of frontotemporal lobar degeneration (FTLD) and dementia with Lewy bodies (DLB) are well known to neurologists and psychiatrists. However, the accuracy of the clinical diagnosis of these diseases in autopsy series is not always adequate. For example, FTLD is a syndrome rather than a clinicopathological disease entity that is comprised of various pathological substrates, including Pick's disease, FTLD with microtubule‐associated protein tau gene mutation, FTLD with tau‐negative ubiquitin‐positive inclusions (FTLD‐U), FTLD‐U with progranulin gene mutation, corticobasal degeneration, basophilic inclusion body disease, and neuronal intermediate filament inclusion disease. Whether these underlying pathologies can be identified clinically is one of the greatest interests in neuropathological research. The pathophysiological relationship between Lewy pathology and Alzheimer pathology in DLB is explored with interest because it may be associated with the accuracy of clinical diagnoses. For example, although Lewy pathology may progress from the brain stem nuclei to the cerebral cortex in Parkinson's disease, recent studies have demonstrated that the progression pattern in DLB is not always identical to that in Parkinson's disease. It is also considered that the progression pattern of Lewy pathology correlates with the evolution of clinical symptoms and that the progression pattern of Lewy pathology may be altered when Alzheimer pathology coexists. In the present paper, the clinicopathological features of two demented cases are presented, and some pathological issues associated with the clinical diagnosis of FTLD and DLB are discussed.
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DOI: 10.1111/j.1479-8301.2009.00286.x
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For example, although Lewy pathology may progress from the brain stem nuclei to the cerebral cortex in Parkinson's disease, recent studies have demonstrated that the progression pattern in DLB is not always identical to that in Parkinson's disease. It is also considered that the progression pattern of Lewy pathology correlates with the evolution of clinical symptoms and that the progression pattern of Lewy pathology may be altered when Alzheimer pathology coexists. 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Email: <email>oyokota1@yahoo.co.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PSYG.PSYG286.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 1 September 2008; accepted 30 November 2008.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="91"></count><count type="wordTotal" number="7566"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Frontotemporal lobar degeneration and dementia with Lewy bodies: Clinicopathological issues associated with antemortem diagnosis</title><title type="shortAuthors">O. Yokota</title><title type="short">Antemortem diagnosis of FTLD and DLB</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>Osamu</givenNames><familyName>YOKOTA</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="JP"><unparsedAffiliation>Department of Neuropathology, Tokyo Institute of Psychiatry, Tokyo, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Alzheimer's disease</keyword><keyword xml:id="k2">α‐internexin</keyword><keyword xml:id="k3">Lewy body</keyword><keyword xml:id="k4">neurofilament</keyword><keyword xml:id="k5">tau</keyword><keyword xml:id="k6">TDP‐43</keyword><keyword xml:id="k7">ubiquitin</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Currently, the clinical diagnostic criteria of frontotemporal lobar degeneration (FTLD) and dementia with Lewy bodies (DLB) are well known to neurologists and psychiatrists. However, the accuracy of the clinical diagnosis of these diseases in autopsy series is not always adequate. For example, FTLD is a syndrome rather than a clinicopathological disease entity that is comprised of various pathological substrates, including Pick's disease, FTLD with microtubule‐associated protein tau gene mutation, FTLD with tau‐negative ubiquitin‐positive inclusions (FTLD‐U), FTLD‐U with progranulin gene mutation, corticobasal degeneration, basophilic inclusion body disease, and neuronal intermediate filament inclusion disease. Whether these underlying pathologies can be identified clinically is one of the greatest interests in neuropathological research. The pathophysiological relationship between Lewy pathology and Alzheimer pathology in DLB is explored with interest because it may be associated with the accuracy of clinical diagnoses. For example, although Lewy pathology may progress from the brain stem nuclei to the cerebral cortex in Parkinson's disease, recent studies have demonstrated that the progression pattern in DLB is not always identical to that in Parkinson's disease. It is also considered that the progression pattern of Lewy pathology correlates with the evolution of clinical symptoms and that the progression pattern of Lewy pathology may be altered when Alzheimer pathology coexists. In the present paper, the clinicopathological features of two demented cases are presented, and some pathological issues associated with the clinical diagnosis of FTLD and DLB are discussed.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>This review article was presented by the author in Symposium of the 23rd annual meeting of Japanese Psychogeriatric Society in Kobe, 27–28 June 2008.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Frontotemporal lobar degeneration and dementia with Lewy bodies: Clinicopathological issues associated with antemortem diagnosis</title></titleInfo><titleInfo type="abbreviated"><title>Antemortem diagnosis of FTLD and DLB</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Frontotemporal lobar degeneration and dementia with Lewy bodies: Clinicopathological issues associated with antemortem diagnosis</title></titleInfo><name type="personal"><namePart type="given">Osamu</namePart><namePart type="family">YOKOTA</namePart><affiliation>Department of Neuropathology, Tokyo Institute of Psychiatry, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Asia</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2009-06</dateIssued><edition>Received 1 September 2008; accepted 30 November 2008.</edition><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="references">91</extent><extent unit="words">7566</extent></physicalDescription><abstract lang="en">Currently, the clinical diagnostic criteria of frontotemporal lobar degeneration (FTLD) and dementia with Lewy bodies (DLB) are well known to neurologists and psychiatrists. However, the accuracy of the clinical diagnosis of these diseases in autopsy series is not always adequate. For example, FTLD is a syndrome rather than a clinicopathological disease entity that is comprised of various pathological substrates, including Pick's disease, FTLD with microtubule‐associated protein tau gene mutation, FTLD with tau‐negative ubiquitin‐positive inclusions (FTLD‐U), FTLD‐U with progranulin gene mutation, corticobasal degeneration, basophilic inclusion body disease, and neuronal intermediate filament inclusion disease. Whether these underlying pathologies can be identified clinically is one of the greatest interests in neuropathological research. The pathophysiological relationship between Lewy pathology and Alzheimer pathology in DLB is explored with interest because it may be associated with the accuracy of clinical diagnoses. For example, although Lewy pathology may progress from the brain stem nuclei to the cerebral cortex in Parkinson's disease, recent studies have demonstrated that the progression pattern in DLB is not always identical to that in Parkinson's disease. It is also considered that the progression pattern of Lewy pathology correlates with the evolution of clinical symptoms and that the progression pattern of Lewy pathology may be altered when Alzheimer pathology coexists. In the present paper, the clinicopathological features of two demented cases are presented, and some pathological issues associated with the clinical diagnosis of FTLD and DLB are discussed.</abstract><subject lang="en"><genre>Keywords</genre><topic>Alzheimer's disease</topic><topic>α‐internexin</topic><topic>Lewy body</topic><topic>neurofilament</topic><topic>tau</topic><topic>TDP‐43</topic><topic>ubiquitin</topic></subject><relatedItem type="host"><titleInfo><title>Psychogeriatrics</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1346-3500</identifier><identifier type="eISSN">1479-8301</identifier><identifier type="DOI">10.1111/(ISSN)1479-8301</identifier><identifier type="PublisherID">PSYG</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>91</start><end>102</end><total>12</total></extent></part></relatedItem><identifier type="istex">7434757C107745856340CED459B977D660ECE2D7</identifier><identifier type="DOI">10.1111/j.1479-8301.2009.00286.x</identifier><identifier type="ArticleID">PSYG286</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 The Author; Journal compilation © 2009 Japanese Psychogeriatric Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Asia</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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