Apolipoprotein E in Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex: genotype analysis and relationships to neuropathological changes.
Identifieur interne : 001595 ( PubMed/Corpus ); précédent : 001594; suivant : 001596Apolipoprotein E in Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex: genotype analysis and relationships to neuropathological changes.
Auteurs : L. Buée ; J. Pérez-Tur ; B. Leveugle ; V. Buée-Scherrer ; E J Mufson ; A J Loerzel ; M C Chartier-Harlin ; D P Perl ; A. Delacourte ; P R HofSource :
- Acta neuropathologica [ 0001-6322 ] ; 1996.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Amyotrophic Lateral Sclerosis (genetics), Amyotrophic Lateral Sclerosis (pathology), Apolipoproteins E (analysis), Apolipoproteins E (genetics), Dementia (genetics), Dementia (pathology), Genotype, Guam, Humans, Immunohistochemistry, Middle Aged, Neurofibrillary Tangles (pathology), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), tau Proteins (analysis).
- MESH :
- chemical , analysis : Apolipoproteins E, tau Proteins.
- geographic : Guam.
- genetics : Amyotrophic Lateral Sclerosis, Apolipoproteins E, Dementia, Parkinson Disease.
- metabolism : Parkinson Disease.
- pathology : Amyotrophic Lateral Sclerosis, Dementia, Neurofibrillary Tangles, Parkinson Disease.
- Aged, Aged, 80 and over, Genotype, Humans, Immunohistochemistry, Middle Aged.
Abstract
Apolipoprotein E (Apo E) has been recently identified within amyloid deposits and neurofibrillary tangles in the brains of Alzheimer's disease (AD) patients. A strong association of the Apo E epsilon 4 allele with higher risk of developing AD has also been reported. In the present study, the distribution of Apo E and the possible relationship between Apo E alleles and neuropathological alterations were analyzed in a series of Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) cases, a neurodegenerative condition characterized neuropathologically by widespread, severe neurofibrillary tangle formation but rare amyloid deposits. ApoE immunoreactivity was consistently observed in both type of lesions in these cases. Compared to tau protein immunoreactivity, there were generally fewer Apo E-immunoreactive neurofibrillary tangles, particularly in the deep layers of the neocortex and in the hippocampus. Genotype analysis revealed that the epsilon 4 allele frequency was 5.9%, the epsilon 3 allele frequency 88.2%, and the epsilon 2 allele frequency 5.9% in this series. Recent data suggest that the Apo E4 variant may induce amyloidogenesis, while E2 could have a neuroprotective role. However, the rare Guamanian patients with amyloid deposits in cortical areas were not related to the epsilon 4 allele, since all cases with senile plaques were epsilon 3/epsilon 3. In addition, compared to unaffected Guamanian cases and other Asian-Pacific populations previously reported, the observed low frequency of the epsilon 2 allele in the present cases, which may be consistent with the notion that this allele, may represent a neuroprotective factor in several neurodegenerative disorders. The present data indicate that there is a strong interaction between Apo E deposition and neurofibrillary changes in Guamanian ALS-PDC.
PubMed: 8834536
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Apolipoprotein E in Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex: genotype analysis and relationships to neuropathological changes.</title><author><name sortKey="Buee, L" sort="Buee, L" uniqKey="Buee L" first="L" last="Buée">L. Buée</name><affiliation><nlm:affiliation>INSERM U422, Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Perez Tur, J" sort="Perez Tur, J" uniqKey="Perez Tur J" first="J" last="Pérez-Tur">J. Pérez-Tur</name></author><author><name sortKey="Leveugle, B" sort="Leveugle, B" uniqKey="Leveugle B" first="B" last="Leveugle">B. Leveugle</name></author><author><name sortKey="Buee Scherrer, V" sort="Buee Scherrer, V" uniqKey="Buee Scherrer V" first="V" last="Buée-Scherrer">V. Buée-Scherrer</name></author><author><name sortKey="Mufson, E J" sort="Mufson, E J" uniqKey="Mufson E" first="E J" last="Mufson">E J Mufson</name></author><author><name sortKey="Loerzel, A J" sort="Loerzel, A J" uniqKey="Loerzel A" first="A J" last="Loerzel">A J Loerzel</name></author><author><name sortKey="Chartier Harlin, M C" sort="Chartier Harlin, M C" uniqKey="Chartier Harlin M" first="M C" last="Chartier-Harlin">M C Chartier-Harlin</name></author><author><name sortKey="Perl, D P" sort="Perl, D P" uniqKey="Perl D" first="D P" last="Perl">D P Perl</name></author><author><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name></author><author><name sortKey="Hof, P R" sort="Hof, P R" uniqKey="Hof P" first="P R" last="Hof">P R Hof</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8834536</idno><idno type="pmid">8834536</idno><idno type="wicri:Area/PubMed/Corpus">001595</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001595</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Apolipoprotein E in Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex: genotype analysis and relationships to neuropathological changes.</title><author><name sortKey="Buee, L" sort="Buee, L" uniqKey="Buee L" first="L" last="Buée">L. Buée</name><affiliation><nlm:affiliation>INSERM U422, Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Perez Tur, J" sort="Perez Tur, J" uniqKey="Perez Tur J" first="J" last="Pérez-Tur">J. Pérez-Tur</name></author><author><name sortKey="Leveugle, B" sort="Leveugle, B" uniqKey="Leveugle B" first="B" last="Leveugle">B. Leveugle</name></author><author><name sortKey="Buee Scherrer, V" sort="Buee Scherrer, V" uniqKey="Buee Scherrer V" first="V" last="Buée-Scherrer">V. Buée-Scherrer</name></author><author><name sortKey="Mufson, E J" sort="Mufson, E J" uniqKey="Mufson E" first="E J" last="Mufson">E J Mufson</name></author><author><name sortKey="Loerzel, A J" sort="Loerzel, A J" uniqKey="Loerzel A" first="A J" last="Loerzel">A J Loerzel</name></author><author><name sortKey="Chartier Harlin, M C" sort="Chartier Harlin, M C" uniqKey="Chartier Harlin M" first="M C" last="Chartier-Harlin">M C Chartier-Harlin</name></author><author><name sortKey="Perl, D P" sort="Perl, D P" uniqKey="Perl D" first="D P" last="Perl">D P Perl</name></author><author><name sortKey="Delacourte, A" sort="Delacourte, A" uniqKey="Delacourte A" first="A" last="Delacourte">A. Delacourte</name></author><author><name sortKey="Hof, P R" sort="Hof, P R" uniqKey="Hof P" first="P R" last="Hof">P R Hof</name></author></analytic><series><title level="j">Acta neuropathologica</title><idno type="ISSN">0001-6322</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Amyotrophic Lateral Sclerosis (genetics)</term><term>Amyotrophic Lateral Sclerosis (pathology)</term><term>Apolipoproteins E (analysis)</term><term>Apolipoproteins E (genetics)</term><term>Dementia (genetics)</term><term>Dementia (pathology)</term><term>Genotype</term><term>Guam</term><term>Humans</term><term>Immunohistochemistry</term><term>Middle Aged</term><term>Neurofibrillary Tangles (pathology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>tau Proteins (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Apolipoproteins E</term><term>tau Proteins</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Guam</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Apolipoproteins E</term><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Dementia</term><term>Neurofibrillary Tangles</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Genotype</term><term>Humans</term><term>Immunohistochemistry</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apolipoprotein E (Apo E) has been recently identified within amyloid deposits and neurofibrillary tangles in the brains of Alzheimer's disease (AD) patients. A strong association of the Apo E epsilon 4 allele with higher risk of developing AD has also been reported. In the present study, the distribution of Apo E and the possible relationship between Apo E alleles and neuropathological alterations were analyzed in a series of Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) cases, a neurodegenerative condition characterized neuropathologically by widespread, severe neurofibrillary tangle formation but rare amyloid deposits. ApoE immunoreactivity was consistently observed in both type of lesions in these cases. Compared to tau protein immunoreactivity, there were generally fewer Apo E-immunoreactive neurofibrillary tangles, particularly in the deep layers of the neocortex and in the hippocampus. Genotype analysis revealed that the epsilon 4 allele frequency was 5.9%, the epsilon 3 allele frequency 88.2%, and the epsilon 2 allele frequency 5.9% in this series. Recent data suggest that the Apo E4 variant may induce amyloidogenesis, while E2 could have a neuroprotective role. However, the rare Guamanian patients with amyloid deposits in cortical areas were not related to the epsilon 4 allele, since all cases with senile plaques were epsilon 3/epsilon 3. In addition, compared to unaffected Guamanian cases and other Asian-Pacific populations previously reported, the observed low frequency of the epsilon 2 allele in the present cases, which may be consistent with the notion that this allele, may represent a neuroprotective factor in several neurodegenerative disorders. The present data indicate that there is a strong interaction between Apo E deposition and neurofibrillary changes in Guamanian ALS-PDC.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8834536</PMID><DateCreated><Year>1996</Year><Month>12</Month><Day>10</Day></DateCreated><DateCompleted><Year>1996</Year><Month>12</Month><Day>10</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0001-6322</ISSN><JournalIssue CitedMedium="Print"><Volume>91</Volume><Issue>3</Issue><PubDate><Year>1996</Year></PubDate></JournalIssue><Title>Acta neuropathologica</Title><ISOAbbreviation>Acta Neuropathol.</ISOAbbreviation></Journal><ArticleTitle>Apolipoprotein E in Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex: genotype analysis and relationships to neuropathological changes.</ArticleTitle><Pagination><MedlinePgn>247-53</MedlinePgn></Pagination><Abstract><AbstractText>Apolipoprotein E (Apo E) has been recently identified within amyloid deposits and neurofibrillary tangles in the brains of Alzheimer's disease (AD) patients. A strong association of the Apo E epsilon 4 allele with higher risk of developing AD has also been reported. In the present study, the distribution of Apo E and the possible relationship between Apo E alleles and neuropathological alterations were analyzed in a series of Guamanian amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) cases, a neurodegenerative condition characterized neuropathologically by widespread, severe neurofibrillary tangle formation but rare amyloid deposits. ApoE immunoreactivity was consistently observed in both type of lesions in these cases. Compared to tau protein immunoreactivity, there were generally fewer Apo E-immunoreactive neurofibrillary tangles, particularly in the deep layers of the neocortex and in the hippocampus. Genotype analysis revealed that the epsilon 4 allele frequency was 5.9%, the epsilon 3 allele frequency 88.2%, and the epsilon 2 allele frequency 5.9% in this series. Recent data suggest that the Apo E4 variant may induce amyloidogenesis, while E2 could have a neuroprotective role. However, the rare Guamanian patients with amyloid deposits in cortical areas were not related to the epsilon 4 allele, since all cases with senile plaques were epsilon 3/epsilon 3. In addition, compared to unaffected Guamanian cases and other Asian-Pacific populations previously reported, the observed low frequency of the epsilon 2 allele in the present cases, which may be consistent with the notion that this allele, may represent a neuroprotective factor in several neurodegenerative disorders. The present data indicate that there is a strong interaction between Apo E deposition and neurofibrillary changes in Guamanian ALS-PDC.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Buée</LastName><ForeName>L</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>INSERM U422, Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pérez-Tur</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Leveugle</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Buée-Scherrer</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Mufson</LastName><ForeName>E J</ForeName><Initials>EJ</Initials></Author><Author ValidYN="Y"><LastName>Loerzel</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Chartier-Harlin</LastName><ForeName>M C</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Perl</LastName><ForeName>D P</ForeName><Initials>DP</Initials></Author><Author ValidYN="Y"><LastName>Delacourte</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Hof</LastName><ForeName>P R</ForeName><Initials>PR</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="N"><Grant><GrantID>AG05138</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG08802</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG09466</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Acta Neuropathol</MedlineTA><NlmUniqueID>0412041</NlmUniqueID><ISSNLinking>0001-6322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001057">Apolipoproteins E</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001057" MajorTopicYN="N">Apolipoproteins E</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003704" MajorTopicYN="N">Dementia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006141" MajorTopicYN="N" Type="Geographic">Guam</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016874" MajorTopicYN="N">Neurofibrillary Tangles</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8834536</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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