Distinct distribution of apolipoprotein E and β-amyloid immunoreactivity in the hippocampus of Parkinson dementia complex of Guam
Identifieur interne : 003E58 ( Main/Exploration ); précédent : 003E57; suivant : 003E59Distinct distribution of apolipoprotein E and β-amyloid immunoreactivity in the hippocampus of Parkinson dementia complex of Guam
Auteurs : Claudia Schwab [États-Unis] ; John C. Steele ; Haruhiko Akiyama ; Patrick L. Mcgeer [États-Unis]Source :
- Acta Neuropathologica [ 0001-6322 ] ; 1996-09-01.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Alzheimer Disease (immunology), Alzheimer disease, Amyloid, Amyloid beta-Peptides (analysis), Amyotrophic Lateral Sclerosis (immunology), Apolipoprotein E, Apolipoproteins E (analysis), Comparative study, Dementia (immunology), Guam (epidemiology), Guam Parkinson dementia, Hippocampus, Hippocampus (immunology), Human, Humans, Immunoblotting, Immunoblotting assay, Immunohistochemistry, Middle Aged, Neurofibrillary tangle, Parkinson Disease (immunology).
- MESH :
- chemical , analysis : Amyloid beta-Peptides, Apolipoproteins E.
- geographic , epidemiology : Guam.
- immunology : Alzheimer Disease, Amyotrophic Lateral Sclerosis, Dementia, Hippocampus, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Humans, Immunoblotting, Immunohistochemistry, Middle Aged.
Abstract
Abstract: The distribution of apolipoprotein E (ApoE) was studied in the brain tissue of cases of the amyotrophic lateral sclerosis – parkinsonism – dementia complex of Guam, locally known as lytico bodig disease (LB), and compared with cases of Alzheimer’s disease (AD) and normal brain tissue. In both LB and AD, strong ApoE immunostaining was observed in association with pathological lesions. In LB, these were mainly extracellular neurofibrillary tangles (eNFTs) which were intensely immunopositive for ApoE. Occasional diffuse β-amyloid protein (βAP) deposits appear in this disorder and they were moderately immunopositive. In AD, senile plaques and diffuse βAP deposits were intensely immunopositive, while eNFTs were only moderately immunopositive. The reason for the strong association of ApoE with the pathological entities in LB and AD is unknown, but may be related to a scavenger function which does not involve lipid metabolism. In both LB and AD, subpial and layer I diffuse deposits were ApoE negative but βAP positive. Intracellular NFTs were mostly ApoE negative. A few showed weak positive staining. These data suggest that ApoE appears in LB and AD pathological lesions only after they are well established. In all controls, as well as all LB and AD cases, strong ApoE immunoreactivity was observed in unidentifiable structures in capillaries. Weak staining in a few neurons and very weak staining of an occasional astrocyte was observed. The source of ApoE which is deposited on extracellular pathological structures in LB and AD is unknown.
Url:
DOI: 10.1007/s004010050533
Affiliations:
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Le document en format XML
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<term>Alzheimer disease</term>
<term>Amyloid</term>
<term>Amyloid beta-Peptides (analysis)</term>
<term>Amyotrophic Lateral Sclerosis (immunology)</term>
<term>Apolipoprotein E</term>
<term>Apolipoproteins E (analysis)</term>
<term>Comparative study</term>
<term>Dementia (immunology)</term>
<term>Guam (epidemiology)</term>
<term>Guam Parkinson dementia</term>
<term>Hippocampus</term>
<term>Hippocampus (immunology)</term>
<term>Human</term>
<term>Humans</term>
<term>Immunoblotting</term>
<term>Immunoblotting assay</term>
<term>Immunohistochemistry</term>
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<term>Neurofibrillary tangle</term>
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<term>Amyotrophic Lateral Sclerosis</term>
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<term>Hippocampus</term>
<term>Parkinson Disease</term>
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<term>Aged</term>
<term>Aged, 80 and over</term>
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<term>Immunohistochemistry</term>
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<term>Etude comparative</term>
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<term>Homme</term>
<term>Immunohistochimie</term>
<term>Méthode immunoblotting</term>
<term>Parkinson démence ile de Guam</term>
<term>Structure neurofibrillaire</term>
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<front><div type="abstract" xml:lang="en">Abstract: The distribution of apolipoprotein E (ApoE) was studied in the brain tissue of cases of the amyotrophic lateral sclerosis – parkinsonism – dementia complex of Guam, locally known as lytico bodig disease (LB), and compared with cases of Alzheimer’s disease (AD) and normal brain tissue. In both LB and AD, strong ApoE immunostaining was observed in association with pathological lesions. In LB, these were mainly extracellular neurofibrillary tangles (eNFTs) which were intensely immunopositive for ApoE. Occasional diffuse β-amyloid protein (βAP) deposits appear in this disorder and they were moderately immunopositive. In AD, senile plaques and diffuse βAP deposits were intensely immunopositive, while eNFTs were only moderately immunopositive. The reason for the strong association of ApoE with the pathological entities in LB and AD is unknown, but may be related to a scavenger function which does not involve lipid metabolism. In both LB and AD, subpial and layer I diffuse deposits were ApoE negative but βAP positive. Intracellular NFTs were mostly ApoE negative. A few showed weak positive staining. These data suggest that ApoE appears in LB and AD pathological lesions only after they are well established. In all controls, as well as all LB and AD cases, strong ApoE immunoreactivity was observed in unidentifiable structures in capillaries. Weak staining in a few neurons and very weak staining of an occasional astrocyte was observed. The source of ApoE which is deposited on extracellular pathological structures in LB and AD is unknown.</div>
</front>
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