Influence of the prion protein and the apolipoprotein E genotype on the Creutzfeldt–Jakob Disease phenotype
Section snippets
Acknowledgements
We would like to thank Dr Bratosiewich and Professor Dr P. Liberski of the Medical University of Lodz and the members of the Belgian CJD study group for their co-operation: Professor Dr J. De Reuck, Professor Dr M. Deprez, Dr A. Michotte, Professor Dr M. Praet, Professor Dr I. Salmon, Professor Dr J.J. Vanderhaeghen, Professor Dr G. Ebinger, Professor Dr J. De Bleecker, Professor Dr R. Sciot, Professor Dr R. Dom, Professor Dr J.M. Brucher and Professor Dr C. Sindic. This research was supported
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Sample preparation from paraffin embedded tissue
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2023, Computational and Structural Biotechnology JournalAPOE gene polymorphisms and susceptibility to Creutzfeldt-Jakob disease
2014, Journal of Clinical NeuroscienceCitation Excerpt :There has been an obvious controversy in the research surrounding CJD that is due to differences in race, study design, selection criteria of patients, and sample sizes. While a significantly higher frequency of APOE 4 allele carriers in CJD patients has been reported compared to controls [28,33–35], other studies have found no significant differences in the APOE genotypes or the APOE 4 allele frequencies between CJD patients and controls [23,29–32]. APOE may be one candidate endogenous factor that affects the risk of developing CJD.
Elevated levels of tau protein in cerebrospinal fluid of patients with probable Creutzfeldt-Jakob disease
2010, American Journal of the Medical SciencesCitation Excerpt :CSF samples were obtained by standard clinical procedures and were free of blood contamination. The PRNP genes of the patients were amplified with a protocol described elsewhere20 and sequenced to determine the codon 129 genotype and to exclude the genetic CJD cases. Protein 14-3-3 positivity in CSF was performed according to the previously published method.21
Clinical and therapeutic aspects of prion disease
2008, Handbook of Clinical NeurologyCitation Excerpt :False‐negative results have also been described and some explanations suggested. A lower sensitivity was found in CJD with a longer disease duration and heterozygosity at codon 129 of the prion protein gene (Zerr et al., 2000b; Van Everbroeck et al., 2001; Castellani et al., 2004). The origin of 14‐3‐3 in the CSF is still unknown.
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