{"title":"阿尔茨海默病和非痴呆老年人斑块中β -淀粉样蛋白的分布","authors":"Shan-Shan Zhan , Robert Veerhuis , Wouter Kamphorst , Piet Eikelenboom","doi":"10.1016/1055-8330(95)90018-7","DOIUrl":null,"url":null,"abstract":"<div><p>Recent studies have shown that cerebral beta amyloid (Aβ) protein deposition is a necessary, but not sufficient, factor to develop the pathology of Alzheimer's disease (AD). In the present immunohistochemical study, we have investigated in AD the distribution of Aβ associated proteins in the cerebral neocortex, in the cerebellar cortex where Aβ plaques are mainly of the diffuse type, and also in the cerebral neocortex of non-demented patients with Aβ plaques. Results show that immunolabeling for C1q, C4c, C3d, α1-ACT and Apolipoprotein E (ApoE) occurs in the great majority of Aβ plaques in all groups. ApoJ is present in Aβ plaques of the cerebral neocortex in AD and in non-demented elderly, but is almost absent from those of the AD cerebellar cortex. C4Bp and P-component, in contrast to AD, rarely occurs in Aβ plaques of the cerebral neocortex in the non-demented elderly. Heparan sulphate proteoglycan (HSPG) core protein and intercellular adhesion molecule-1 (ICAM-1) are absent in the diffuse Aβ plaques in the AD cerebellum. These differences in distribution and expression of Aβ associated proteins may be determined by brain region specific factors (cerebral cortex versus cerebellar cortex) and clinical state (demented versus non-demented cases). We suggest that, besides Aβ peptide, certain Aβ associated proteins are required for both amyloid plaque formation and for the induction of neurofibrillary changes.</p></div>","PeriodicalId":19127,"journal":{"name":"Neurodegeneration","volume":"4 3","pages":"Pages 291-297"},"PeriodicalIF":0.0000,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/1055-8330(95)90018-7","citationCount":"82","resultStr":"{\"title\":\"Distribution of beta amyloid associated proteins in plaques in Alzheimer's disease and in the non-demented elderly\",\"authors\":\"Shan-Shan Zhan , Robert Veerhuis , Wouter Kamphorst , Piet Eikelenboom\",\"doi\":\"10.1016/1055-8330(95)90018-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Recent studies have shown that cerebral beta amyloid (Aβ) protein deposition is a necessary, but not sufficient, factor to develop the pathology of Alzheimer's disease (AD). In the present immunohistochemical study, we have investigated in AD the distribution of Aβ associated proteins in the cerebral neocortex, in the cerebellar cortex where Aβ plaques are mainly of the diffuse type, and also in the cerebral neocortex of non-demented patients with Aβ plaques. Results show that immunolabeling for C1q, C4c, C3d, α1-ACT and Apolipoprotein E (ApoE) occurs in the great majority of Aβ plaques in all groups. ApoJ is present in Aβ plaques of the cerebral neocortex in AD and in non-demented elderly, but is almost absent from those of the AD cerebellar cortex. C4Bp and P-component, in contrast to AD, rarely occurs in Aβ plaques of the cerebral neocortex in the non-demented elderly. Heparan sulphate proteoglycan (HSPG) core protein and intercellular adhesion molecule-1 (ICAM-1) are absent in the diffuse Aβ plaques in the AD cerebellum. These differences in distribution and expression of Aβ associated proteins may be determined by brain region specific factors (cerebral cortex versus cerebellar cortex) and clinical state (demented versus non-demented cases). We suggest that, besides Aβ peptide, certain Aβ associated proteins are required for both amyloid plaque formation and for the induction of neurofibrillary changes.</p></div>\",\"PeriodicalId\":19127,\"journal\":{\"name\":\"Neurodegeneration\",\"volume\":\"4 3\",\"pages\":\"Pages 291-297\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/1055-8330(95)90018-7\",\"citationCount\":\"82\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurodegeneration\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/1055833095900187\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurodegeneration","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/1055833095900187","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Distribution of beta amyloid associated proteins in plaques in Alzheimer's disease and in the non-demented elderly
Recent studies have shown that cerebral beta amyloid (Aβ) protein deposition is a necessary, but not sufficient, factor to develop the pathology of Alzheimer's disease (AD). In the present immunohistochemical study, we have investigated in AD the distribution of Aβ associated proteins in the cerebral neocortex, in the cerebellar cortex where Aβ plaques are mainly of the diffuse type, and also in the cerebral neocortex of non-demented patients with Aβ plaques. Results show that immunolabeling for C1q, C4c, C3d, α1-ACT and Apolipoprotein E (ApoE) occurs in the great majority of Aβ plaques in all groups. ApoJ is present in Aβ plaques of the cerebral neocortex in AD and in non-demented elderly, but is almost absent from those of the AD cerebellar cortex. C4Bp and P-component, in contrast to AD, rarely occurs in Aβ plaques of the cerebral neocortex in the non-demented elderly. Heparan sulphate proteoglycan (HSPG) core protein and intercellular adhesion molecule-1 (ICAM-1) are absent in the diffuse Aβ plaques in the AD cerebellum. These differences in distribution and expression of Aβ associated proteins may be determined by brain region specific factors (cerebral cortex versus cerebellar cortex) and clinical state (demented versus non-demented cases). We suggest that, besides Aβ peptide, certain Aβ associated proteins are required for both amyloid plaque formation and for the induction of neurofibrillary changes.