Inga Zerr

TL;DR: The present data demonstrate the existence of six phenotypic variants of sCJD, and the physicochemical properties of PrPSc in conjunction with the PRNP codon 129 genotype largely determine this phenotypesic variability, and allow a molecular classification of the disease variants.

TL;DR: Cerebral cortical signal increase and high signal in caudate nucleus and putamen on fluid attenuated inversion recovery or diffusion-weight imaging magnetic resonance imaging are useful in the diagnosis of sporadic Creutzfeldt–Jakob disease.

TL;DR: In this paper, a comparison of clinical and neuropathologic diagnoses and evaluation of the sensitivity and specificity of EEG and 14-3-3 CSF immunoassay were conducted.

TL;DR: CSF analysis for 14‐3‐3 protein should thus be performed in any case suspect for CJD, as false‐positive results in a single CSF analysis were seen in patients with herpes simplex encephalitis, hypoxic brain damage, atypical enphalitis, intracerebral metastases of a bronchial carcinoma, metabolic encephalopathy, and progressive dementia of unknown cause.

TL;DR: The authors' results show that clinicopathological phenotypes include genetic Creutzfeldt–Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann–Sträussler–Scheinker disease (GSS).