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Update on Creutzfeldt-Jakob disease
Current Opinion in Neurology, 2004Prion diseases are transmissible fatal neurodegenerative disorders in which infectivity is associated with the accumulation of PrP(Sc), a disease-related isoform of normal cellular prion protein. The recent emergence of variant Creutzfeldt-Jakob disease has led to major public health concerns, and the need for the development of effective treatments ...
Giovanna, Mallucci, John, Collinge
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Familial Creutzfeldt-Jakob disease
Journal of the Neurological Sciences, 1979A Finnish family is described with 9 cases of presenile dementia in 3 generations. The mean age at onset was 52 years (range 46--62 years). Progressive dementia, upper motor neuron signs, muscular rigidity, and twitching, irregular tremors were consistent features in the 6 clinically investigated patients and were associated with spongiform change in ...
M, Haltia +4 more
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Creutzfeldt‐Jakob disease in Mexico
Neuropathology, 2007Creutzfeldt‐Jakob disease (CJD) is classified within the group of transmissible spongiform encephalopathies (TSE). It is a rapidly progressive illness that affects mental functions. The average age of onset is 50 years. Various tests can help orient the clinical diagnosis, but the confirmatory test is still the post mortem analysis.
Leora, Velásquez-Pérez +4 more
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Iatrogenic Creutzfeldt-Jakob disease
Alzheimer Disease & Associated Disorders, 1987Over the past 2 years, Creutzfeldt-Jakob disease (CJD) has affected several patients who received cadaver pituitary-derived growth hormone (pit-hGH) and one patient who received a cadaveric dura mater graft. The risk of iatrogenic transmission of CJD has long been recognized, but until recently, the low prevalence of the disorder and minimal use of ...
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Unilateral Creutzfeldt‐Jakob disease
Neurology, 1986A 73-year-old woman had progressive right hemiparesis, aphasia, and focal motor seizures. EEG showed periodic discharges on the left. She died 8 weeks after onset. At autopsy, there was marked spongiform change, neuronal loss, and severe proliferation of astrocytes predominantly on the left and most prominently in the insular and centroparietal cortex.
H, Yamanouchi, H, Budka, K, Vass
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MRI in Creutzfeldt-Jakob Disease
Neurology, 1996To the Editor: We read with great interest the recent article by Yoon et al. [1] concerning a 47-year-old woman with a pathologically proven case of Creutzfeldt-Jakob disease (CJD), with prominent asymmetry in abnormal high signal intensity of the basal ganglia on T2-weighted and proton density-weighted MRIs. They concluded that symmetric or asymmetric
K, Takamiya, Y, Iwasaki, M, Kinoshita
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Epidemiology of Creutzfeldt-Jakob disease
British Medical Bulletin, 1993Extensive information on the epidemiology of Creutzfeldt-Jakob Disease (CJD) has accumulated since the original transmission of CJD to primates in 1968. One aim of this research was to discover the mechanism of natural transmission of CJD but the epidemiological evidence virtually precludes case to case transmission as a causative mechanism, except in ...
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Precautions for Creutzfeldt-Jakob Disease
Infection Control, 1982Creutzfeldt-Jakob disease (CJD) is a rapidly progressive, fatal disease of the central nervous system. Premortem diagnosis may or may not be conclusive. Because the etiologic agent is virulent, definition of necessary precautions for medical staff associated with such patients is needed.
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Variant Creutzfeldt–Jakob disease
2018Variant CJD (vCJD) was described first in the United Kingdom in 1996. It is a zoonotic form of human prion disease, originating from dietary contamination of human food with material from bovine spongiform encephalopathy (BSE)-affected cattle. It has important epidemiologic, clinical, and neuropathogic differences from other forms of human prion ...
Jean-Philippe, Brandel, Richard, Knight
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Creutzfeldt‐Jakob disease in Japan
Neurology, 1983In a nationwide survey of Creutzfeldt-Jakob disease (CJD) in Japan, the point prevalence rate on June 1, 1978 in Fukuoka Prefecture and the estimated national prevalence rate were approximately one per one million population. The minimal period prevalence rate was 0.45 per one million population.
S, Tsuji, Y, Kuroiwa
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