Comparison of β-protein/A4 deposits and Alz-50-stained cytoskeletal changes in the hypothalamus and adjoining areas of Alzheimer's disease patients : amorphic plaques and cytoskeletal changes occur independently
Alzheimer's disease is characterized neuropathologically by senile plaques and cytoskeletal changes. It has been proposed that amorphic plaques would locally induce anterograde propagation of cytoskeletal changes in consecutive neurons followed by amorphic plaque deposition at their axonal term...
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Veröffentlicht in: | Acta neuropathologica 1998-08, Vol.96 (2), p.129-138 |
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description | Alzheimer's disease is characterized neuropathologically by senile plaques and cytoskeletal changes. It has been proposed that amorphic plaques would locally induce anterograde propagation of cytoskeletal changes in consecutive neurons followed by amorphic plaque deposition at their axonal terminals. The Alzheimer changes would spread in this way along neural pathways. To test the 'primary amyloid anatomical cascade hypothesis', Congo red staining, beta-protein/A4 (Abeta) antiserum and Alz-50, which recognizes cytoskeletal changes, were applied to the hypothalamus and adjoining brain areas of five Alzheimer's disease patients of 40-90 years of age and five age- and sex-matched controls. The results showed that (1) virtually all Abeta plaques in the hypothalamus were of the Congo red-negative amorphic type; (2) amorphic plaques and Alz-50-stained cytokeletal changes were observed not only in all Alzheimer's disease patients but also in a non-demented, 90-year-old control subject; (3) the density of amorphic plaques in the hypothalamus was unrelated to the duration of the dementia; (4) the density of amorphic plaques was unrelated to that of Alz-50-stained cytoskeletal changes; (5) double-labeling with anti-Abeta and Alz-50 did not show an evident topical relationship between amorphic plaque deposition and the occurrence of cytoskeletal changes; and (6) the distribution of Abeta and Alz-50 staining in five brain areas, for which essential anatomical information is available, did not support the primary amyloid anatomical cascade hypothesis. Amorphic plaques and cytoskeletal changes rather occur independently. |
doi_str_mv | 10.1007/s004010050872 |
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A. P ; KAMPHORST, W ; RAVID, R ; SWAAB, D. F</creator><creatorcontrib>VAN DE NES, J. A. P ; KAMPHORST, W ; RAVID, R ; SWAAB, D. F</creatorcontrib><description>Alzheimer's disease is characterized neuropathologically by senile plaques and cytoskeletal changes. It has been proposed that amorphic plaques would locally induce anterograde propagation of cytoskeletal changes in consecutive neurons followed by amorphic plaque deposition at their axonal terminals. The Alzheimer changes would spread in this way along neural pathways. To test the 'primary amyloid anatomical cascade hypothesis', Congo red staining, beta-protein/A4 (Abeta) antiserum and Alz-50, which recognizes cytoskeletal changes, were applied to the hypothalamus and adjoining brain areas of five Alzheimer's disease patients of 40-90 years of age and five age- and sex-matched controls. The results showed that (1) virtually all Abeta plaques in the hypothalamus were of the Congo red-negative amorphic type; (2) amorphic plaques and Alz-50-stained cytokeletal changes were observed not only in all Alzheimer's disease patients but also in a non-demented, 90-year-old control subject; (3) the density of amorphic plaques in the hypothalamus was unrelated to the duration of the dementia; (4) the density of amorphic plaques was unrelated to that of Alz-50-stained cytoskeletal changes; (5) double-labeling with anti-Abeta and Alz-50 did not show an evident topical relationship between amorphic plaque deposition and the occurrence of cytoskeletal changes; and (6) the distribution of Abeta and Alz-50 staining in five brain areas, for which essential anatomical information is available, did not support the primary amyloid anatomical cascade hypothesis. Amorphic plaques and cytoskeletal changes rather occur independently.</description><identifier>ISSN: 0001-6322</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s004010050872</identifier><identifier>PMID: 9705127</identifier><identifier>CODEN: ANPTAL</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid ; Amyloid beta-Peptides - metabolism ; Antigens - metabolism ; Biological and medical sciences ; Brain ; Coloring Agents ; Cytoskeleton ; Cytoskeleton - pathology ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dementia disorders ; Female ; Humans ; Hypothalamus ; Hypothalamus - metabolism ; Hypothalamus - pathology ; Hypotheses ; Male ; Medical sciences ; Middle Aged ; Nerve Tissue Proteins - metabolism ; Neurodegenerative diseases ; Neurology ; Plaque, Amyloid - pathology ; Senile plaques</subject><ispartof>Acta neuropathologica, 1998-08, Vol.96 (2), p.129-138</ispartof><rights>1998 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 1998.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c345t-caad2f6054b7966fb24b8cedb37313adaacf9e03a84e23d2d1611b1d4ebe57293</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2313279$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9705127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VAN DE NES, J. A. P</creatorcontrib><creatorcontrib>KAMPHORST, W</creatorcontrib><creatorcontrib>RAVID, R</creatorcontrib><creatorcontrib>SWAAB, D. F</creatorcontrib><title>Comparison of β-protein/A4 deposits and Alz-50-stained cytoskeletal changes in the hypothalamus and adjoining areas of Alzheimer's disease patients : amorphic plaques and cytoskeletal changes occur independently</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><description>Alzheimer's disease is characterized neuropathologically by senile plaques and cytoskeletal changes. It has been proposed that amorphic plaques would locally induce anterograde propagation of cytoskeletal changes in consecutive neurons followed by amorphic plaque deposition at their axonal terminals. The Alzheimer changes would spread in this way along neural pathways. To test the 'primary amyloid anatomical cascade hypothesis', Congo red staining, beta-protein/A4 (Abeta) antiserum and Alz-50, which recognizes cytoskeletal changes, were applied to the hypothalamus and adjoining brain areas of five Alzheimer's disease patients of 40-90 years of age and five age- and sex-matched controls. The results showed that (1) virtually all Abeta plaques in the hypothalamus were of the Congo red-negative amorphic type; (2) amorphic plaques and Alz-50-stained cytokeletal changes were observed not only in all Alzheimer's disease patients but also in a non-demented, 90-year-old control subject; (3) the density of amorphic plaques in the hypothalamus was unrelated to the duration of the dementia; (4) the density of amorphic plaques was unrelated to that of Alz-50-stained cytoskeletal changes; (5) double-labeling with anti-Abeta and Alz-50 did not show an evident topical relationship between amorphic plaque deposition and the occurrence of cytoskeletal changes; and (6) the distribution of Abeta and Alz-50 staining in five brain areas, for which essential anatomical information is available, did not support the primary amyloid anatomical cascade hypothesis. Amorphic plaques and cytoskeletal changes rather occur independently.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Antigens - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Coloring Agents</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - pathology</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dementia disorders</subject><subject>Female</subject><subject>Humans</subject><subject>Hypothalamus</subject><subject>Hypothalamus - metabolism</subject><subject>Hypothalamus - pathology</subject><subject>Hypotheses</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Plaque, Amyloid - pathology</subject><subject>Senile plaques</subject><issn>0001-6322</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkcuKFDEUhgtRxp7RpUshoIyrcnKr2-yaxhsMuNF1cSo5NZU2lZRJatE-lg_iygcyTTcDipvkJPny_yf5i-IFo28Zpc1NpFTSXFW0bfijYsOk4CWthHhcbCilrKwF50-Lyxj3ecUbWV0UF11Dq1xvit87Py8QTPSO-JH8-lkuwSc07mYricbFR5MiAafJ1v4oK1rGBMahJuqQfPyGFhNYoiZw9xiJcSRNSKbD4tMEFub1dBf03htn3D2BgBCPTlluQjNjeBOJNjHvIlkgGXTZ75bA7MMyGUUWC99XPMn819MrtYbsnJvFPLhkD8-KJyPYiM_P81Xx9f27L7uP5d3nD59227tSCVmlUgFoPta0kkPT1fU4cDm0CvUgGsEEaAA1dkgFtBK50FyzmrGBaYkDVg3vxFVxfdLNf3ZsMvWziQqtBYd-jX0jWsm5qDP46h9w79fgcm89l6zKYTRtm6nyRKngYww49kswM4RDz2h_zLr_K-vMvzyrrsOM-oE-h5vPX5_PISqwYwCnTHzAeH4kbzrxB3futiE</recordid><startdate>19980801</startdate><enddate>19980801</enddate><creator>VAN DE NES, J. A. P</creator><creator>KAMPHORST, W</creator><creator>RAVID, R</creator><creator>SWAAB, D. 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A. P ; KAMPHORST, W ; RAVID, R ; SWAAB, D. F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c345t-caad2f6054b7966fb24b8cedb37313adaacf9e03a84e23d2d1611b1d4ebe57293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Antigens - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Coloring Agents</topic><topic>Cytoskeleton</topic><topic>Cytoskeleton - pathology</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dementia disorders</topic><topic>Female</topic><topic>Humans</topic><topic>Hypothalamus</topic><topic>Hypothalamus - metabolism</topic><topic>Hypothalamus - pathology</topic><topic>Hypotheses</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Plaque, Amyloid - pathology</topic><topic>Senile plaques</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VAN DE NES, J. A. P</creatorcontrib><creatorcontrib>KAMPHORST, W</creatorcontrib><creatorcontrib>RAVID, R</creatorcontrib><creatorcontrib>SWAAB, D. 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A. P</au><au>KAMPHORST, W</au><au>RAVID, R</au><au>SWAAB, D. F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of β-protein/A4 deposits and Alz-50-stained cytoskeletal changes in the hypothalamus and adjoining areas of Alzheimer's disease patients : amorphic plaques and cytoskeletal changes occur independently</atitle><jtitle>Acta neuropathologica</jtitle><addtitle>Acta Neuropathol</addtitle><date>1998-08-01</date><risdate>1998</risdate><volume>96</volume><issue>2</issue><spage>129</spage><epage>138</epage><pages>129-138</pages><issn>0001-6322</issn><eissn>1432-0533</eissn><coden>ANPTAL</coden><abstract>Alzheimer's disease is characterized neuropathologically by senile plaques and cytoskeletal changes. It has been proposed that amorphic plaques would locally induce anterograde propagation of cytoskeletal changes in consecutive neurons followed by amorphic plaque deposition at their axonal terminals. The Alzheimer changes would spread in this way along neural pathways. To test the 'primary amyloid anatomical cascade hypothesis', Congo red staining, beta-protein/A4 (Abeta) antiserum and Alz-50, which recognizes cytoskeletal changes, were applied to the hypothalamus and adjoining brain areas of five Alzheimer's disease patients of 40-90 years of age and five age- and sex-matched controls. The results showed that (1) virtually all Abeta plaques in the hypothalamus were of the Congo red-negative amorphic type; (2) amorphic plaques and Alz-50-stained cytokeletal changes were observed not only in all Alzheimer's disease patients but also in a non-demented, 90-year-old control subject; (3) the density of amorphic plaques in the hypothalamus was unrelated to the duration of the dementia; (4) the density of amorphic plaques was unrelated to that of Alz-50-stained cytoskeletal changes; (5) double-labeling with anti-Abeta and Alz-50 did not show an evident topical relationship between amorphic plaque deposition and the occurrence of cytoskeletal changes; and (6) the distribution of Abeta and Alz-50 staining in five brain areas, for which essential anatomical information is available, did not support the primary amyloid anatomical cascade hypothesis. Amorphic plaques and cytoskeletal changes rather occur independently.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>9705127</pmid><doi>10.1007/s004010050872</doi><tpages>10</tpages></addata></record> |
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subjects | Adult Aged Aged, 80 and over Alzheimer Disease - pathology Alzheimer's disease Amyloid Amyloid beta-Peptides - metabolism Antigens - metabolism Biological and medical sciences Brain Coloring Agents Cytoskeleton Cytoskeleton - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia disorders Female Humans Hypothalamus Hypothalamus - metabolism Hypothalamus - pathology Hypotheses Male Medical sciences Middle Aged Nerve Tissue Proteins - metabolism Neurodegenerative diseases Neurology Plaque, Amyloid - pathology Senile plaques |
title | Comparison of β-protein/A4 deposits and Alz-50-stained cytoskeletal changes in the hypothalamus and adjoining areas of Alzheimer's disease patients : amorphic plaques and cytoskeletal changes occur independently |
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