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Striation is the characteristic neuritic abnormality in Alzheimer disease
In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic str...
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Published in: | Brain research 1998-12, Vol.813 (2), p.329-333 |
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creator | Velasco, Manuel E. Smith, Mark A. Siedlak, Sandra L. Nunomura, Akihiko Perry, George |
description | In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity. |
doi_str_mv | 10.1016/S0006-8993(98)01034-8 |
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They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(98)01034-8</identifier><identifier>PMID: 9838181</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer disease ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Argyrophilic grains ; Axonal transport ; Axonal Transport - physiology ; Biological and medical sciences ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Humans ; Image analysis ; Medical sciences ; Microscopy, Electron ; Microtubules - metabolism ; Middle Aged ; Neurites - metabolism ; Neurites - pathology ; Neurites - ultrastructure ; Neurofibrillary tangles ; Neurofibrillary Tangles - pathology ; Neurofibrillary Tangles - ultrastructure ; Neurology ; Neurons - metabolism ; Neurons - pathology ; Neurons - ultrastructure ; Neuropil - pathology ; Neuropil threads ; Synapses - metabolism ; Synapses - pathology</subject><ispartof>Brain research, 1998-12, Vol.813 (2), p.329-333</ispartof><rights>1998 Elsevier Science B.V.</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1998 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-82eab0e7a70dd6a592c66dd9eea2669044de4ea4011aa59d92b1b3eee4c47b73</citedby><cites>FETCH-LOGICAL-c486t-82eab0e7a70dd6a592c66dd9eea2669044de4ea4011aa59d92b1b3eee4c47b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1596223$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9838181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Velasco, Manuel E.</creatorcontrib><creatorcontrib>Smith, Mark A.</creatorcontrib><creatorcontrib>Siedlak, Sandra L.</creatorcontrib><creatorcontrib>Nunomura, Akihiko</creatorcontrib><creatorcontrib>Perry, George</creatorcontrib><title>Striation is the characteristic neuritic abnormality in Alzheimer disease</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer disease</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Argyrophilic grains</subject><subject>Axonal transport</subject><subject>Axonal Transport - physiology</subject><subject>Biological and medical sciences</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Humans</subject><subject>Image analysis</subject><subject>Medical sciences</subject><subject>Microscopy, Electron</subject><subject>Microtubules - metabolism</subject><subject>Middle Aged</subject><subject>Neurites - metabolism</subject><subject>Neurites - pathology</subject><subject>Neurites - ultrastructure</subject><subject>Neurofibrillary tangles</subject><subject>Neurofibrillary Tangles - pathology</subject><subject>Neurofibrillary Tangles - ultrastructure</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurons - ultrastructure</subject><subject>Neuropil - pathology</subject><subject>Neuropil threads</subject><subject>Synapses - metabolism</subject><subject>Synapses - pathology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkE1rHDEMhk1pSTdpf0JgDqU0h2llj8djn0oI_QgEekjuRmNrWZX5SG1vIfn1ncku6TEnWbyPZPEIcS7hswRpvtwCgKmtc80nZy9AQqNr-0pspO1UbZSG12LzjLwVpzn_XtqmcXAiTpxtrLRyI65vS2IsPE8V56rsqAo7TBgKJc6FQzXRPvH6wH6a04gDl4eKp-pyeNwRj5SqyJkw0zvxZotDpvfHeibuvn-7u_pZ3_z6cX11eVMHbU2prSLsgTrsIEaDrVPBmBgdESpjHGgdSRNqkBKXNDrVy74hIh1013fNmfh4WHuf5j97ysWPnAMNA04077PvAKxpTfMiKDsJ0Cq7gO0BDGnOOdHW3yceMT14CX5V7Z9U-9Wjd9Y_qfbr3Pnxg30_UnyeOrpd8g_HHHPAYZtwCpz_L2-dUWq98-sBo0XaX6bkc2CaAkVOFIqPM79wyD8Lopty</recordid><startdate>19981207</startdate><enddate>19981207</enddate><creator>Velasco, Manuel E.</creator><creator>Smith, Mark A.</creator><creator>Siedlak, Sandra L.</creator><creator>Nunomura, Akihiko</creator><creator>Perry, George</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19981207</creationdate><title>Striation is the characteristic neuritic abnormality in Alzheimer disease</title><author>Velasco, Manuel E. ; Smith, Mark A. ; Siedlak, Sandra L. ; Nunomura, Akihiko ; Perry, George</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-82eab0e7a70dd6a592c66dd9eea2669044de4ea4011aa59d92b1b3eee4c47b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer disease</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Argyrophilic grains</topic><topic>Axonal transport</topic><topic>Axonal Transport - physiology</topic><topic>Biological and medical sciences</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Humans</topic><topic>Image analysis</topic><topic>Medical sciences</topic><topic>Microscopy, Electron</topic><topic>Microtubules - metabolism</topic><topic>Middle Aged</topic><topic>Neurites - metabolism</topic><topic>Neurites - pathology</topic><topic>Neurites - ultrastructure</topic><topic>Neurofibrillary tangles</topic><topic>Neurofibrillary Tangles - pathology</topic><topic>Neurofibrillary Tangles - ultrastructure</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neurons - ultrastructure</topic><topic>Neuropil - pathology</topic><topic>Neuropil threads</topic><topic>Synapses - metabolism</topic><topic>Synapses - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Velasco, Manuel E.</creatorcontrib><creatorcontrib>Smith, Mark A.</creatorcontrib><creatorcontrib>Siedlak, Sandra L.</creatorcontrib><creatorcontrib>Nunomura, Akihiko</creatorcontrib><creatorcontrib>Perry, George</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Velasco, Manuel E.</au><au>Smith, Mark A.</au><au>Siedlak, Sandra L.</au><au>Nunomura, Akihiko</au><au>Perry, George</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Striation is the characteristic neuritic abnormality in Alzheimer disease</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1998-12-07</date><risdate>1998</risdate><volume>813</volume><issue>2</issue><spage>329</spage><epage>333</epage><pages>329-333</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>9838181</pmid><doi>10.1016/S0006-8993(98)01034-8</doi><tpages>5</tpages></addata></record> |
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subjects | Aged Aged, 80 and over Alzheimer disease Alzheimer Disease - metabolism Alzheimer Disease - pathology Argyrophilic grains Axonal transport Axonal Transport - physiology Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Humans Image analysis Medical sciences Microscopy, Electron Microtubules - metabolism Middle Aged Neurites - metabolism Neurites - pathology Neurites - ultrastructure Neurofibrillary tangles Neurofibrillary Tangles - pathology Neurofibrillary Tangles - ultrastructure Neurology Neurons - metabolism Neurons - pathology Neurons - ultrastructure Neuropil - pathology Neuropil threads Synapses - metabolism Synapses - pathology |
title | Striation is the characteristic neuritic abnormality in Alzheimer disease |
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