C‐reactive protein and IL‐6: new marker proteins for the diagnosis of CJD in plasma?

Völkel, Dirk; Zimmermann, Klaus F.; Zerr, Inga; Lindner, Thomas; Bodemer, Monika; Poser, S.; Schwarz, Hans

doi:10.1046/j.1537-2995.2001.41121509.x

Cited by 26 publications

(14 citation statements)

References 46 publications

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“…Il a également été décrit une élévation de la CRP et de l'IL6 chez 70 à 80 % des patients atteints de MCJ sporadique [1]. Cette élévation n'est malheureusement pas d'un très grand secours dans le diagnostic, en raison de son manque de spéci-ficité.…”

Section: Diagnostic Au Laboratoireunclassified

Diagnostic des maladies à prions humaines: quel rôle pour le biologiste?

Peoc’h

Hébert

Chasseigneaux

et al. 2006

Immuno-analyse & Biologie Spécialisée

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Section: Diagnostic Au Laboratoireunclassified

Diagnostic des maladies à prions humaines: quel rôle pour le biologiste?

Peoc’h

Hébert

Chasseigneaux

et al. 2006

Immuno-analyse & Biologie Spécialisée

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“…Völkel et al [120] recently identified two potential markers, C-reactive protein (CRP) and interleukin 6 (IL-6) in the plasma of sporadic CJD subjects. Expression of CRP and IL-6 in CJD patients were compared to proteins S100 and NSE which have previously been reported as markers of CJD in human plasma [77,91,119].…”

Section: 110c-reactive Protein and Interleukinmentioning

confidence: 99%

“…Expression of CRP and IL-6 in CJD patients were compared to proteins S100 and NSE which have previously been reported as markers of CJD in human plasma [77,91,119]. According to Völkel et al [120], CRP identified 78.3% of a group of 46 subjects with sCJD as positive for the disease, while IL-6 identified 73.3%, and NSE and S100 identified 13% and 76.1% of the patients respectively. These results indicate that CJD gives rise to CRP, IL-6 and S100 in blood plasma as a consequence of neuronal and tissue damage during CJD.…”

Section: 110c-reactive Protein and Interleukinmentioning

confidence: 99%

The use of non-prion biomarkers for the diagnosis of Transmissible Spongiform Encephalopathies in the live animal

Parveen

Moorby²,

Allison³

et al. 2005

Vet. Res.

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-Scrapie and bovine spongiform encephalopathy (BSE) are major global concerns and the emergence of variant Creutzfeldt-Jakob disease (vCJD) has caused turmoil for blood transfusion services and hospitals worldwide. Recent reports of iatrogenic CJD (iCJD) cases following blood transfusions from Transmissible Spongiform Encephalopathies (TSE)-infected donors have fuelled this concern. Major diagnostic tests for BSE and scrapie are conducted post-mortem from animals in late stages of the disease. Although the lymphoreticular system is involved in the earlier pathogenesis of some forms of sheep scrapie and vCJD, which presents great opportunity for diagnostic development, other TSE diseases (some strains of scrapie, sporadic CJD (sCJD) and bovine BSE) do not present such a diagnostic opportunity. Thus, there is an urgent need for premortem tests that differentiate between healthy and diseased individuals at early stages of illness, in accessible samples such as blood and urine using less invasive procedures. This review reports on the current state of progress in the development and use of prion and non-prion biomarkers in the diagnosis of TSE diseases. Some of these efforts have concentrated on improving the sensitivity of PrP Sc detection to allow in vivo diagnosis at low abundances of PrP Sc whilst others have sought to identify non-prion protein biomarkers of TSE disease, many of which are still at early stages of development. In this review we comment upon the limitations of prion based tests and review current research on the development of tests for TSE that rely on non-prion disease markers in body fluids that may allow preclinical disease diagnosis.

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“…A study of plasma samples analysed with tests specific for C-reactive protein (CRP), IL-6, NSE, S-100 proteins and PrP C concluded that these have only a limited value in the diagnosis of CJD, although a combination of markers might improve the specificity (Volkel et al 2001). Increased heat shock protein 70 mRNA levels in mononuclear blood cells is also an auxiliary tool for the diagnosis of sCJD (Shyu et al 2000).…”

Section: Blood and Serummentioning

confidence: 99%

Rationale for diagnosing human prion disease

Kovács

Voigtländer

Gelpí

et al. 2004

The World Journal of Biological Psychiatry

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Human prion diseases (PrD) like Creutzfeldt-Jakob disease (CJD) include sporadic, acquired and familial neurodegenerative disorders. The central events in the neuropathological process of PrDs are severe neuronal loss, spongiform change and accumulation of abnormal prion protein (PrPSc). The latter is a conformational variant of the host-encoded cellular PrP (PrPC), a copper-binding protein. The physiological role of PrPC is debated. Definitive diagnosis of PrD is based on post mortem demonstration of PrPSc by immunohistochemistry or Western blot. Mutations in the PrP gene (PRNP), the polymorphic site at codon 129, and the molecular characteristic of protease resistant PrP influence the phenotype. Clinical symptoms, cranial MRI scan, EEG and investigation of 14-3-3 protein in cerebrospinal fluid (CSF) suggest a diagnosis of probable CJD. Variant CJD, related to bovine spongiform encephalopathy, shows a different clinical course, symmetrical high intensity MRI signal in the pulvinar, presence of PrPSc in tonsil biopsy tissue, and a lower sensitivity of CSF 14-3-3 protein compared to sporadic CJD. Future possibilities in diagnosis of PrDs include either the demonstration of PrPSc in body fluids or disease associated changes in laboratory variables or gene expression.

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C‐reactive protein and IL‐6: new marker proteins for the diagnosis of CJD in plasma?

Cited by 26 publications

References 46 publications

Diagnostic des maladies à prions humaines: quel rôle pour le biologiste?

Diagnostic des maladies à prions humaines: quel rôle pour le biologiste?

The use of non-prion biomarkers for the diagnosis of Transmissible Spongiform Encephalopathies in the live animal

Rationale for diagnosing human prion disease

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