ArticleJournal of Alzheimer's disease : JAD2017
Diagnostic Accuracy of a Combined Analysis of Cerebrospinal Fluid t-PrP, t-tau, p-tau, and Aβ42 in the Differential Diagnosis of Creutzfeldt-Jakob Disease from Alzheimer's Disease with Emphasis on Atypical Disease Variants.
Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
- Cellular prion protein and its derived peptides: multifaceted roles in neurodegenerative diseases and potential as biomarkers.Cell & bioscience · 2026Review
- Biological Fluid Biomarkers in Human Prion Diseases with a Note on Biosafety.Sub-cellular biochemistry · 2025Review
- FDG-PET patterns associate with survival in patients with prion disease.Annals of clinical and translational neurology · 2024Article
- Molecular Biomarkers of Neurodegenerative Disorders: A Practical Guide to Their Appropriate Use and Interpretation in Clinical Practice.International journal of molecular sciences · 2024Review
- 14-3-3 proteins-a moonlight protein complex with therapeutic potential in neurological disorder: in-depth review with Alzheimer's disease.Frontiers in molecular biosciences · 2024Review
- Diagnosis in Scrapie: Conventional Methods and New Biomarkers.Pathogens (Basel, Switzerland) · 2023Review
- Diagnostic and prognostic value of cerebrospinal fluid SNAP-25 and neurogranin in Creutzfeldt-Jakob disease in a clinical setting cohort of rapidly progressive dementias.Alzheimer's research & therapy · 2023Article
- Real-time quaking-induced conversion assays for prions: Applying a sensitive but imperfect test in clinical practice.European journal of neurology · 2023Article
- Comparative evaluation of clinical and cerebrospinal fluid biomarker characteristics in rapidly and non-rapidly progressive Alzheimer's disease.Alzheimer's research & therapy · 2023Observational
- Sporadic Creutzfeldt-Jakob disease as a mimic of progressive supranuclear palsy.Acta neurologica Belgica · 2022Article
- Regional variability and genotypic and pharmacodynamic effects on PrP concentration in the CNS.JCI insight · 2022Article
- Comparison of cerebrospinal fluid tau, ptau(181), synuclein, and 14-3-3 for the detection of Creutzfeldt-Jakob disease in clinical practice.Journal of neural transmission (Vienna, Austria : 1996) · 2022Article
- Article
- Neuronal ER-Signalosome Proteins as Early Biomarkers in Prodromal Alzheimer's Disease Independent of Amyloid-β Production and Tau Phosphorylation.Frontiers in molecular neuroscience · 2022Article
- Biomarkers and diagnostic guidelines for sporadic Creutzfeldt-Jakob disease.The Lancet. Neurology · 2021Review
- Prion protein oligomers cause neuronal cytoskeletal damage in rapidly progressive Alzheimer's disease.Molecular neurodegeneration · 2021Article
- Cerebrospinal fluid and plasma biomarkers in individuals at risk for genetic prion disease.BMC medicine · 2020Article
- Detection of Pathognomonic Biomarker PrPBiomolecules · 2020Review
- Domain-specific Quantification of Prion Protein in Cerebrospinal Fluid by Targeted Mass Spectrometry.Molecular & cellular proteomics : MCP · 2019Article
- Prion protein quantification in human cerebrospinal fluid as a tool for prion disease drug development.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to recent studies, the determination of cerebrospinal fluid (CSF) total tau (t-tau)/phosphorylated tau (p-tau) ratio and total prion protein (t-PrP) levels significantly improves the accuracy of the diagnosis of Alzheimer's disease (AD) in atypical cases with clinical or laboratory features mimicking Creutzfeldt-Jakob disease (CJD). However, this has neither been validated nor tested in series including atypical CJD variants. Furthermore, the added diagnostic value of amyloid-β (Aβ)42 remains unclear. To address these issues, we measured t-PrP, 14-3-3, t-tau, p-tau, and Aβ42 CSF levels in 45 typical and 44 atypical/rapidly progressive AD patients, 54 typical and 54 atypical CJD patients, and 33 controls. CJD patients showed significantly lower CSF t-PrP levels than controls and AD patients. Furthermore, atypical CJD was associated with lower t-PrP levels in comparison to typical CJD. T-tau, 14-3-3, or t-PrP alone yielded, respectively, 80.6, 63.0, and 73.0% sensitivity and 75.3, 92.1, and 75% specificity in distinguishing AD from CJD. On receiver operating characteristic (ROC) curve analyses of biomarker combinations, the (t-tau×Aβ42)/(p-tau×t-PrP) ratio achieved the best accuracy, with 98.1% sensitivity and 97.7% specificity overall, and 96.2% sensitivity and 95.5% specificity for the "atypical" disease groups. Our results show that the combined analysis of CSF t-PrP, t-tau, p-tau, and Aβ42 is clinically useful in the differential diagnosis between CJD and AD. Furthermore, the finding of reduced CSF t-PrP levels in CJD patients suggest that, likewise Aβ42 in AD, CSF t-PrP levels reflect the extent of PrPc conversion into abnormal PrP (PrPSc) and the burden of PrPSc deposition in CJD.
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