Neocortical Synapse Density and Braak Stage in the Lewy Body Variant of Alzheimer Disease: A Comparison with Classic Alzheimer Disease and Normal Aging
Substantial numbers of cortical and subcortical Lewy bodies are seen in approximately one quarter of patients whose brains show sufficient histopathologic changes for a neuropathologic diagnosis of definite Alzheimer disease (AD). This subset of cases has been named the Lewy body variant of AD (LBV)...
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| Veröffentlicht in: | Journal of neuropathology and experimental neurology 1998-10, Vol.57 (10), p.955-960 |
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| container_title | Journal of neuropathology and experimental neurology |
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| creator | Brown, Daniel F Risser, Richard C Bigio, Eileen H Tripp, Patrick Stiegler, Ashley Welch, Erin Eagan, Kathleen P Hladik, Christa L White, Charles L |
| description | Substantial numbers of cortical and subcortical Lewy bodies are seen in approximately one quarter of patients whose brains show sufficient histopathologic changes for a neuropathologic diagnosis of definite Alzheimer disease (AD). This subset of cases has been named the Lewy body variant of AD (LBV). Despite comparable dementia and the presence of neocortical senile plaques in LBV patients, the overall burden of neuropathologic changes, in particular neurofibrillary tangles (NET), is less than in classic AD. While NFT frequency correlates with dementia severity in classic AD, the cognitive impairment in patients with LBV cannot be completely explained by such changes. Since several studies have suggested a role for synapse loss in relation to dementia severity in classic AD, we decided to investigate the role of synapse loss as a candidate for the cognitive impairment of LBV.The Braak staging method is based upon the distribution and severity of neurofibrillary changes, and one therefore would expect LBV cases to be assigned to lower Braak stages. In the present study we assigned a Braak stage to 14 LBV cases, 31 classic AD cases, and a group of 10 non-demented aged controls. We compared the severity of synapse loss as determined by ELISA immunoassay for synaptophysin and Braak stage among the three diagnostic groups. When compared to normal controls, synaptophysin concentrations were statistically significantly lower in both demented groups. There was comparable synapse loss in LBV and AD despite significantly lower Braak stages in the LBV cases. These results suggest a major role for loss of synapses as the substrate of cognitive impairment in LBV. |
| doi_str_mv | 10.1097/00005072-199810000-00007 |
| format | Article |
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This subset of cases has been named the Lewy body variant of AD (LBV). Despite comparable dementia and the presence of neocortical senile plaques in LBV patients, the overall burden of neuropathologic changes, in particular neurofibrillary tangles (NET), is less than in classic AD. While NFT frequency correlates with dementia severity in classic AD, the cognitive impairment in patients with LBV cannot be completely explained by such changes. Since several studies have suggested a role for synapse loss in relation to dementia severity in classic AD, we decided to investigate the role of synapse loss as a candidate for the cognitive impairment of LBV.The Braak staging method is based upon the distribution and severity of neurofibrillary changes, and one therefore would expect LBV cases to be assigned to lower Braak stages. In the present study we assigned a Braak stage to 14 LBV cases, 31 classic AD cases, and a group of 10 non-demented aged controls. We compared the severity of synapse loss as determined by ELISA immunoassay for synaptophysin and Braak stage among the three diagnostic groups. When compared to normal controls, synaptophysin concentrations were statistically significantly lower in both demented groups. There was comparable synapse loss in LBV and AD despite significantly lower Braak stages in the LBV cases. These results suggest a major role for loss of synapses as the substrate of cognitive impairment in LBV.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/00005072-199810000-00007</identifier><identifier>PMID: 9786245</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Advertising executives ; Aged ; Aging - pathology ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Analysis ; Biological and medical sciences ; Brain ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Diagnosis ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Immunohistochemistry ; Lewy Bodies - metabolism ; Lewy Bodies - pathology ; Lewy Bodies - ultrastructure ; Male ; Medical sciences ; Neocortex - metabolism ; Neocortex - pathology ; Neocortex - ultrastructure ; Neurology ; Severity of Illness Index ; Synapses - metabolism ; Synapses - pathology ; Synapses - ultrastructure ; Synaptophysin - metabolism ; Ubiquitins</subject><ispartof>Journal of neuropathology and experimental neurology, 1998-10, Vol.57 (10), p.955-960</ispartof><rights>1998 American Association of Neuropathologists, Inc</rights><rights>1998 INIST-CNRS</rights><rights>COPYRIGHT 1998 Oxford University Press</rights><rights>Copyright American Association of Neuropathologists, Inc. Oct 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5007-73fc1229901e494ef08f18da7855650bd3046a8786f352853e330da6b4f960d3</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=2411951$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9786245$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, Daniel F</creatorcontrib><creatorcontrib>Risser, Richard C</creatorcontrib><creatorcontrib>Bigio, Eileen H</creatorcontrib><creatorcontrib>Tripp, Patrick</creatorcontrib><creatorcontrib>Stiegler, Ashley</creatorcontrib><creatorcontrib>Welch, Erin</creatorcontrib><creatorcontrib>Eagan, Kathleen P</creatorcontrib><creatorcontrib>Hladik, Christa L</creatorcontrib><creatorcontrib>White, Charles L</creatorcontrib><title>Neocortical Synapse Density and Braak Stage in the Lewy Body Variant of Alzheimer Disease: A Comparison with Classic Alzheimer Disease and Normal Aging</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>Substantial numbers of cortical and subcortical Lewy bodies are seen in approximately one quarter of patients whose brains show sufficient histopathologic changes for a neuropathologic diagnosis of definite Alzheimer disease (AD). This subset of cases has been named the Lewy body variant of AD (LBV). Despite comparable dementia and the presence of neocortical senile plaques in LBV patients, the overall burden of neuropathologic changes, in particular neurofibrillary tangles (NET), is less than in classic AD. While NFT frequency correlates with dementia severity in classic AD, the cognitive impairment in patients with LBV cannot be completely explained by such changes. Since several studies have suggested a role for synapse loss in relation to dementia severity in classic AD, we decided to investigate the role of synapse loss as a candidate for the cognitive impairment of LBV.The Braak staging method is based upon the distribution and severity of neurofibrillary changes, and one therefore would expect LBV cases to be assigned to lower Braak stages. In the present study we assigned a Braak stage to 14 LBV cases, 31 classic AD cases, and a group of 10 non-demented aged controls. We compared the severity of synapse loss as determined by ELISA immunoassay for synaptophysin and Braak stage among the three diagnostic groups. When compared to normal controls, synaptophysin concentrations were statistically significantly lower in both demented groups. There was comparable synapse loss in LBV and AD despite significantly lower Braak stages in the LBV cases. These results suggest a major role for loss of synapses as the substrate of cognitive impairment in LBV.</description><subject>Advertising executives</subject><subject>Aged</subject><subject>Aging - pathology</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Analysis</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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Prion diseases</topic><topic>Diagnosis</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lewy Bodies - metabolism</topic><topic>Lewy Bodies - pathology</topic><topic>Lewy Bodies - ultrastructure</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neocortex - metabolism</topic><topic>Neocortex - pathology</topic><topic>Neocortex - ultrastructure</topic><topic>Neurology</topic><topic>Severity of Illness Index</topic><topic>Synapses - metabolism</topic><topic>Synapses - pathology</topic><topic>Synapses - ultrastructure</topic><topic>Synaptophysin - metabolism</topic><topic>Ubiquitins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, Daniel F</creatorcontrib><creatorcontrib>Risser, Richard C</creatorcontrib><creatorcontrib>Bigio, Eileen H</creatorcontrib><creatorcontrib>Tripp, Patrick</creatorcontrib><creatorcontrib>Stiegler, Ashley</creatorcontrib><creatorcontrib>Welch, Erin</creatorcontrib><creatorcontrib>Eagan, Kathleen P</creatorcontrib><creatorcontrib>Hladik, Christa L</creatorcontrib><creatorcontrib>White, Charles L</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Proquest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Daniel F</au><au>Risser, Richard C</au><au>Bigio, Eileen H</au><au>Tripp, Patrick</au><au>Stiegler, Ashley</au><au>Welch, Erin</au><au>Eagan, Kathleen P</au><au>Hladik, Christa L</au><au>White, Charles L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neocortical Synapse Density and Braak Stage in the Lewy Body Variant of Alzheimer Disease: A Comparison with Classic Alzheimer Disease and Normal Aging</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>1998-10</date><risdate>1998</risdate><volume>57</volume><issue>10</issue><spage>955</spage><epage>960</epage><pages>955-960</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>Substantial numbers of cortical and subcortical Lewy bodies are seen in approximately one quarter of patients whose brains show sufficient histopathologic changes for a neuropathologic diagnosis of definite Alzheimer disease (AD). This subset of cases has been named the Lewy body variant of AD (LBV). Despite comparable dementia and the presence of neocortical senile plaques in LBV patients, the overall burden of neuropathologic changes, in particular neurofibrillary tangles (NET), is less than in classic AD. While NFT frequency correlates with dementia severity in classic AD, the cognitive impairment in patients with LBV cannot be completely explained by such changes. Since several studies have suggested a role for synapse loss in relation to dementia severity in classic AD, we decided to investigate the role of synapse loss as a candidate for the cognitive impairment of LBV.The Braak staging method is based upon the distribution and severity of neurofibrillary changes, and one therefore would expect LBV cases to be assigned to lower Braak stages. In the present study we assigned a Braak stage to 14 LBV cases, 31 classic AD cases, and a group of 10 non-demented aged controls. We compared the severity of synapse loss as determined by ELISA immunoassay for synaptophysin and Braak stage among the three diagnostic groups. When compared to normal controls, synaptophysin concentrations were statistically significantly lower in both demented groups. There was comparable synapse loss in LBV and AD despite significantly lower Braak stages in the LBV cases. These results suggest a major role for loss of synapses as the substrate of cognitive impairment in LBV.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>9786245</pmid><doi>10.1097/00005072-199810000-00007</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals |
| subjects | Advertising executives Aged Aging - pathology Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Analysis Biological and medical sciences Brain Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Diagnosis Enzyme-Linked Immunosorbent Assay Female Humans Immunohistochemistry Lewy Bodies - metabolism Lewy Bodies - pathology Lewy Bodies - ultrastructure Male Medical sciences Neocortex - metabolism Neocortex - pathology Neocortex - ultrastructure Neurology Severity of Illness Index Synapses - metabolism Synapses - pathology Synapses - ultrastructure Synaptophysin - metabolism Ubiquitins |
| title | Neocortical Synapse Density and Braak Stage in the Lewy Body Variant of Alzheimer Disease: A Comparison with Classic Alzheimer Disease and Normal Aging |
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