Research Topics
Genomes and GenesSpecies | P BrownSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
|
Detail Information
Publications
The risk of bovine spongiform encephalopathy ('mad cow disease') to human healthP Brown
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
JAMA 278:1008-11. 1997..sheep) or unrecognized bovine spongiform encephalopathy (in cattle), the practice of recycling nonedible sheep and cattle tissue for animal nutrition, and precautionary measures already taken or under consideration by government agencies..- Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt-Jakob disease in humansP Brown
Laboratory of CNS Studies, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 4122, USA
Transfusion 39:1169-78. 1999.... - Phenotype-genotype studies in kuru: implications for new variant Creutzfeldt-Jakob diseaseL Cervenakova
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 95:13239-41. 1998..quot; The clinical phenotype of such cases should be similar to that of homozygous cases, but may have less (or at least less readily identified) amyloid plaque formation... - Creutzfeldt-Jakob disease cosegregates with the codon 178Asn PRNP mutation in families of European originL G Goldfarb
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892
Ann Neurol 31:274-81. 1992..Linkage analysis in two informative families yielded a lod score of 5.30, which, because no recombinants were found, strongly suggests that codon 178Asn is the actual disease mutation... - APOE in non-Alzheimer amyloidoses: transmissible spongiform encephalopathiesJ Chapman
Clinical Neurogenetics Unit, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 4129, USA
Neurology 51:548-53. 1998..Amyloid formation is an important part of the pathogenesis in AD as well as in spongiform encephalopathies; apoE deposition in amyloid plaques has been documented in both conditions... - Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimentally transmitted diseaseP Brown
Laboratory of CNS Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892
Ann Neurol 35:513-29. 1994.... - Infectious amyloid precursor gene sequences in primates used for experimental transmission of human spongiform encephalopathyL Cervenakova
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892
Proc Natl Acad Sci U S A 91:12159-62. 1994.... - Increased susceptibility to Kuru of carriers of the PRNP 129 methionine/methionine genotypeH S Lee
Clinical Neurogenetics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
J Infect Dis 183:192-196. 2001..These findings are relevant to the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom, because all vCJD patients tested thus far have been M/M carriers... - Novel PRNP sequence variant associated with familial encephalopathyL Cervenakova
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland
Am J Med Genet 88:653-6. 1999..Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:653-656, 1999. Published 1999 Wiley-Liss, Inc... - Infectious cerebral amyloidosis: clinical spectrum, risks and remediesP Brown
Laboratory of CNS Studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD
Dev Biol Stand 80:91-101. 1993..The paper concludes with a discussion of the means by which such risks may be minimized... - Ancestral origins and worldwide distribution of the PRNP 200K mutation causing familial Creutzfeldt-Jakob diseaseH S Lee
Clinical Neurogenetics Unit, National Institute of Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA
Am J Hum Genet 64:1063-70. 1999..On the basis of this study, we conclude that founder effect and independent mutational events are responsible for the current geographic distribution of hereditary CJD associated with the 200K mutation... - Creutzfeldt-Jacob disease associated with the PRNP codon 200Lys mutation: an analysis of 45 familiesL G Goldfarb
Laboratory of CNS Studies, NINDS, NIH, Bethesda, MD 20892
Eur J Epidemiol 7:477-86. 1991.... - Creutzfeldt-Jakob disease and kuru patients lack a mutation consistently found in the Gerstmann-Sträussler-Scheinker syndromeL G Goldfarb
Laboratory of CNS Studies, NINDS, NIH, Bethesda, Maryland 20892
Exp Neurol 108:247-50. 1990.... - Atypical Creutzfeldt-Jakob disease in an American family with an insert mutation in the PRNP amyloid precursor geneP Brown
Laboratory of CNS Studies, NINDS, NIH, Bethesda, MD 20892
Neurology 42:422-7. 1992..Analysis of this and other families with similar inserts suggests that such mutations in the PRNP gene not only predispose to CJD, but also modify its phenotypic expression... - Transmissible familial Creutzfeldt-Jakob disease associated with five, seven, and eight extra octapeptide coding repeats in the PRNP geneL G Goldfarb
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892
Proc Natl Acad Sci U S A 88:10926-30. 1991..These observations, together with data on published British patients with 11 and 14 repeats, strongly suggest that the occurrence of 10 or more octapeptide repeats in the encoded amyloid precursor protein predisposes to CJD... - Microwave treatment enhances the immunostaining of amyloid deposits in both the transmissible and non-transmissible brain amyloidosesP P Liberski
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
Neurodegeneration 5:95-9. 1996..Microwave processing, which is easy to perform and comparatively inexpensive, makes exposure to the potentially toxic fumes of formic acid unnecessary... - Seroprevalence of antibodies to HTLV-I in patients with chronic neurological disorders other than tropical spastic paraparesisC A Mora
Laboratory of Central Nervous System Studies, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892
Ann Neurol 23:S192-5. 1988..The seropositivity of the 7 Jamaican patients with polymyositis requires further study... - The ultrastructural diversity of scrapie-associated fibrils isolated from experimental scrapie and Creutzfeldt-Jakob diseaseP P Liberski
Laboratory of Central Nervous System Studies, NINDS, National Institutes of Health, Bethesda, MD 20892
J Comp Pathol 105:377-86. 1991..Thus, SAF preparations from scrapie-affected hamsters can be ultrastructurally distinguished from those of CJD-affected mice, an observation that presumably reflects differences in their respective host-encoded amyloid protein subunits... - New studies on the heat resistance of hamster-adapted scrapie agent: threshold survival after ashing at 600 degrees C suggests an inorganic template of replicationP Brown
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 97:3418-21. 2000..These results suggest that an inorganic molecular template with a decomposition point near 600 degrees C is capable of nucleating the biological replication of the scrapie agent... - Iatrogenic Creutzfeldt-Jakob disease at the millenniumP Brown
Laboratory of CNS Studies, NINDS, NIH, Bethesda, MD 20892, USA
Neurology 55:1075-81. 2000.... - Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease: background, evolution, and current concernsP Brown
National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
Emerg Infect Dis 7:6-16. 2001..Government agencies in many countries continue to implement new measures to minimize this risk... - The pathogenesis of transmissible spongiform encephalopathy: routes to the brain and the erection of therapeutic barricadesP Brown
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 4122, USA
Cell Mol Life Sci 58:259-65. 2001..Possible modes and sites of therapeutic intervention are suggested... - Creutzfeldt-Jakob disease: blood infectivity and screening testsP Brown
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-4122, USA
Semin Hematol 38:2-6. 2001.... - Fatal familial insomnia and familial Creutzfeldt-Jakob disease: disease phenotype determined by a DNA polymorphismL G Goldfarb
Laboratory of Central Nervous System Studies, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892
Science 258:806-8. 1992..Thus, two distinct disease phenotypes linked to a single pathogenic mutation can be determined by a common polymorphism...