{"title":"人类朊病毒疾病向啮齿动物的传播","authors":"Jun Tateishi","doi":"10.1006/smvy.1996.0022","DOIUrl":null,"url":null,"abstract":"<div><p>PrP genotypes of human prion diseases were closely related to deposition types of PrP<sup>Sc</sup>, clinico-pathologic phenotypes and transmission rates to rodents. Wild type CJD with 129M/M, iatrogenic cases, and hereditary CJD with V1801, E200K, and M232R showed synaptic type deposition of PrP<sup>Sc</sup>, similar phenotypes and, except for V1801, similar transmission rates. One patient with fatal familial insomnia transmitted the disease to mice. Plaque type deposition of PrP<sup>Sc</sup>induced various phenotypes, such as GSS or Alzheimer's disease-like dementia, usually with a longer clinical course than CJD. Experimental transmission was positive from one-third of the cases with P102L but negative from other mutation cases with PrP plaques. Polymorphism at codon 129 may modify phenotypes as well as transmission rates.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 3","pages":"Pages 175-180"},"PeriodicalIF":0.0000,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0022","citationCount":"14","resultStr":"{\"title\":\"Transmission of human prion diseases to rodents\",\"authors\":\"Jun Tateishi\",\"doi\":\"10.1006/smvy.1996.0022\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>PrP genotypes of human prion diseases were closely related to deposition types of PrP<sup>Sc</sup>, clinico-pathologic phenotypes and transmission rates to rodents. Wild type CJD with 129M/M, iatrogenic cases, and hereditary CJD with V1801, E200K, and M232R showed synaptic type deposition of PrP<sup>Sc</sup>, similar phenotypes and, except for V1801, similar transmission rates. One patient with fatal familial insomnia transmitted the disease to mice. Plaque type deposition of PrP<sup>Sc</sup>induced various phenotypes, such as GSS or Alzheimer's disease-like dementia, usually with a longer clinical course than CJD. Experimental transmission was positive from one-third of the cases with P102L but negative from other mutation cases with PrP plaques. Polymorphism at codon 129 may modify phenotypes as well as transmission rates.</p></div>\",\"PeriodicalId\":92955,\"journal\":{\"name\":\"Seminars in virology\",\"volume\":\"7 3\",\"pages\":\"Pages 175-180\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1006/smvy.1996.0022\",\"citationCount\":\"14\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Seminars in virology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1044577396900220\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Seminars in virology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1044577396900220","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
PrP genotypes of human prion diseases were closely related to deposition types of PrPSc, clinico-pathologic phenotypes and transmission rates to rodents. Wild type CJD with 129M/M, iatrogenic cases, and hereditary CJD with V1801, E200K, and M232R showed synaptic type deposition of PrPSc, similar phenotypes and, except for V1801, similar transmission rates. One patient with fatal familial insomnia transmitted the disease to mice. Plaque type deposition of PrPScinduced various phenotypes, such as GSS or Alzheimer's disease-like dementia, usually with a longer clinical course than CJD. Experimental transmission was positive from one-third of the cases with P102L but negative from other mutation cases with PrP plaques. Polymorphism at codon 129 may modify phenotypes as well as transmission rates.
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