C F Lippa, T W Smith, L Nee, Y Robitaille, B Crain, D Dickson, D Pulaski-Salo, D A Pollen
{"title":"家族性阿尔茨海默病与皮质路易体:是否存在遗传易感性因素?","authors":"C F Lippa, T W Smith, L Nee, Y Robitaille, B Crain, D Dickson, D Pulaski-Salo, D A Pollen","doi":"10.1159/000106945","DOIUrl":null,"url":null,"abstract":"<p><p>The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"191-4"},"PeriodicalIF":0.0000,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106945","citationCount":"17","resultStr":"{\"title\":\"Familial Alzheimer's disease and cortical Lewy bodies: is there a genetic susceptibility factor?\",\"authors\":\"C F Lippa, T W Smith, L Nee, Y Robitaille, B Crain, D Dickson, D Pulaski-Salo, D A Pollen\",\"doi\":\"10.1159/000106945\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.</p>\",\"PeriodicalId\":79336,\"journal\":{\"name\":\"Dementia (Basel, Switzerland)\",\"volume\":\"6 4\",\"pages\":\"191-4\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000106945\",\"citationCount\":\"17\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Dementia (Basel, Switzerland)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000106945\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Dementia (Basel, Switzerland)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000106945","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Familial Alzheimer's disease and cortical Lewy bodies: is there a genetic susceptibility factor?
The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.