Biochemical staging of synucleinopathy and amyloid deposition in dementia with Lewy bodies.
Identifieur interne : 000607 ( Ncbi/Merge ); précédent : 000606; suivant : 000608Biochemical staging of synucleinopathy and amyloid deposition in dementia with Lewy bodies.
Auteurs : V. Deramecourt [France] ; S. Bombois ; C-A Maurage ; A. Ghestem ; H. Drobecq ; E. Vanmechelen ; F. Lebert ; F. Pasquier ; A. DelacourteSource :
- Journal of neuropathology and experimental neurology [ 0022-3069 ] ; 2006.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Amyloid beta-Protein Precursor (metabolism), Cerebral Cortex (anatomy & histology), Cerebral Cortex (metabolism), Cerebral Cortex (pathology), Electrophoresis, Gel, Two-Dimensional, Female, Humans, Lewy Body Disease (metabolism), Lewy Body Disease (pathology), Male, Mass Spectrometry, Middle Aged, Parkinson Disease (metabolism), Parkinson Disease (pathology), alpha-Synuclein (metabolism), tau Proteins (metabolism).
- MESH :
- chemical , metabolism : Amyloid beta-Protein Precursor, alpha-Synuclein, tau Proteins.
- anatomy & histology : Cerebral Cortex.
- metabolism : Alzheimer Disease, Cerebral Cortex, Lewy Body Disease, Parkinson Disease.
- pathology : Alzheimer Disease, Cerebral Cortex, Lewy Body Disease, Parkinson Disease.
- Aged, Aged, 80 and over, Electrophoresis, Gel, Two-Dimensional, Female, Humans, Male, Mass Spectrometry, Middle Aged.
Abstract
The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.
DOI: 10.1097/01.jnen.0000205145.54457.ea
PubMed: 16651889
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Deramecourt</name><affiliation wicri:level="3"><nlm:affiliation>Inserm Unit 815, Lille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Inserm Unit 815, Lille</wicri:regionArea><placeName><region type="region">Hauts-de-France</region><region type="old region">Nord-Pas-de-Calais</region><settlement type="city">Lille</settlement></placeName></affiliation></author><author><name sortKey="Bombois, S" sort="Bombois, S" uniqKey="Bombois S" first="S" last="Bombois">S. Bombois</name></author><author><name sortKey="Maurage, C A" sort="Maurage, C A" uniqKey="Maurage C" first="C-A" last="Maurage">C-A Maurage</name></author><author><name sortKey="Ghestem, A" sort="Ghestem, A" uniqKey="Ghestem A" first="A" last="Ghestem">A. Ghestem</name></author><author><name sortKey="Drobecq, H" sort="Drobecq, H" uniqKey="Drobecq H" first="H" last="Drobecq">H. Drobecq</name></author><author><name sortKey="Vanmechelen, E" sort="Vanmechelen, E" uniqKey="Vanmechelen E" first="E" last="Vanmechelen">E. Vanmechelen</name></author><author><name sortKey="Lebert, F" sort="Lebert, F" uniqKey="Lebert F" first="F" last="Lebert">F. Lebert</name></author><author><name sortKey="Pasquier, F" sort="Pasquier, F" uniqKey="Pasquier F" first="F" last="Pasquier">F. Pasquier</name></author><author><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name></author></analytic><series><title level="j">Journal of neuropathology and experimental neurology</title><idno type="ISSN">0022-3069</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (pathology)</term><term>Amyloid beta-Protein Precursor (metabolism)</term><term>Cerebral Cortex (anatomy & histology)</term><term>Cerebral Cortex (metabolism)</term><term>Cerebral Cortex (pathology)</term><term>Electrophoresis, Gel, Two-Dimensional</term><term>Female</term><term>Humans</term><term>Lewy Body Disease (metabolism)</term><term>Lewy Body Disease (pathology)</term><term>Male</term><term>Mass Spectrometry</term><term>Middle Aged</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>alpha-Synuclein (metabolism)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Protein Precursor</term><term>alpha-Synuclein</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Cerebral Cortex</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Cerebral Cortex</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Electrophoresis, Gel, Two-Dimensional</term><term>Female</term><term>Humans</term><term>Male</term><term>Mass Spectrometry</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16651889</PMID><DateCreated><Year>2006</Year><Month>05</Month><Day>02</Day></DateCreated><DateCompleted><Year>2006</Year><Month>06</Month><Day>05</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3069</ISSN><JournalIssue CitedMedium="Print"><Volume>65</Volume><Issue>3</Issue><PubDate><Year>2006</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of neuropathology and experimental neurology</Title><ISOAbbreviation>J. Neuropathol. Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Biochemical staging of synucleinopathy and amyloid deposition in dementia with Lewy bodies.</ArticleTitle><Pagination><MedlinePgn>278-88</MedlinePgn></Pagination><Abstract><AbstractText>The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Deramecourt</LastName><ForeName>V</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Inserm Unit 815, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bombois</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Maurage</LastName><ForeName>C-A</ForeName><Initials>CA</Initials></Author><Author ValidYN="Y"><LastName>Ghestem</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Drobecq</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Vanmechelen</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Lebert</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Pasquier</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Delacourte</LastName><ForeName>A</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neuropathol Exp Neurol</MedlineTA><NlmUniqueID>2985192R</NlmUniqueID><ISSNLinking>0022-3069</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016564">Amyloid beta-Protein Precursor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau 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UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015180" MajorTopicYN="N">Electrophoresis, Gel, Two-Dimensional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020961" MajorTopicYN="N">Lewy Body Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013058" MajorTopicYN="N">Mass Spectrometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>5</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>6</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Bombois</name><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name><name sortKey="Drobecq, H" sort="Drobecq, H" uniqKey="Drobecq H" first="H" last="Drobecq">H. Drobecq</name><name sortKey="Ghestem, A" sort="Ghestem, A" uniqKey="Ghestem A" first="A" last="Ghestem">A. Ghestem</name><name sortKey="Lebert, F" sort="Lebert, F" uniqKey="Lebert F" first="F" last="Lebert">F. Lebert</name><name sortKey="Maurage, C A" sort="Maurage, C A" uniqKey="Maurage C" first="C-A" last="Maurage">C-A Maurage</name><name sortKey="Pasquier, F" sort="Pasquier, F" uniqKey="Pasquier F" first="F" last="Pasquier">F. Pasquier</name><name sortKey="Vanmechelen, E" sort="Vanmechelen, E" uniqKey="Vanmechelen E" first="E" last="Vanmechelen">E. Vanmechelen</name></noCountry><country name="France"><region name="Hauts-de-France"><name sortKey="Deramecourt, V" sort="Deramecourt, V" uniqKey="Deramecourt V" first="V" last="Deramecourt">V. 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