Elevated levels of tau-protein in cerebrospinal fluid of patients with Creutzfeldt–Jakob disease

Otto, Markus; Wiltfang, Jens; Tumani, Hayrettin; Zerr, Inga; Lantsch, Maria; Kornhuber, Johannes; Weber, Thomas K.; Kretzschmar, Hans A.; Poser, S.

doi:10.1016/s0304-3940(97)00215-2

Cited by 305 publications

(178 citation statements)

References 18 publications

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“…CSF-tau, which is used in the present study, has already been validated in several neurodegenerative disorders. 5,6 However, the relevance of a transient increase in CSF-tau to the biology of treatmentrelated neural dysfunction is not known. We are now investigating a putative correlation between the transient increases of CSF-tau during the first phase of treatment with impairments found in neuropsychologic tests after treatment.…”

Section: Discussionmentioning

confidence: 99%

“…36 However, the exploratory nature of this study and availability of CSF-tau as a marker for neurodegeneration [5][6][7] led us to use this test as a first indication for neuronal damage. Upon carrying out NSE determinations in a large subset of these CSF samples, results emerged that were similar to those observed with CSF-tau (unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

“…4 CSF-tau as a marker for neurodegeneration has already been well studied in patients with disorders such as Alzheimer's disease, stroke, and Creutzfeldt-Jakob disease. [5][6][7] We therefore carried out a pilot study to determine whether CSF-tau could be useful to monitor chemotherapy-related neurotoxicity in children being treated for hematological malignancies.…”

Section: Introductionmentioning

confidence: 99%

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Disease- and treatment-related elevation of the neurodegenerative marker tau in children with hematological malignancies

et al. 2000

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Children acquire neuropsychologic dysfunctions after chemotherapy for hematologic malignancy. In this study, putative changes in levels of CSF-tau (a marker of neural dysintegrity) in leukemic children prior to and during chemotherapy were studied. Cerebrospinal fluid (CSF) samples were obtained before and during treatment from patients with B cell non-Hodgkin's lymphoma (NHL, n = 10), non-B cell acute lymphoblastic leukemia/NHL (non-B-ALL, n = 48), acute myeloid leukemia (AML, n = 9), other malignant diseases (n = 9), and six control children. A sandwich-type ELISA (INNOTEST hTAU-Ag) was used for measuring CSF-tau. Sixteen out of 50 patients with hematological malignancies, including the patients with proven leukemic CNS invasion, already showed high CSF-tau levels at baseline (Ͼ300 pg/ml). The pre-induction treatment for non-B-ALL, consisting of only corticosteroids and methotrexate (MTX), resulted in a significant increase of tau at day 8 (on average to 535 pg/ml). Larger increases as compared to baseline levels of CSF-tau were observed in patients treated for B-NHL with systemic vincristine, corticosteroids and cyclophosphamide, and intrathecal MTX (mean 776 pg/ml at day 8). In two AML patients with CNS invasion, CSF-tau increased during chemotherapy up to 1500 and 948 pg/ml, respectively. In one non-B-ALL patient with MTX-induced clinical neurotoxicity, CSF-tau was above the detection limit of 2000 pg/ml. Almost one-third of the patients with hematological malignancies had elevated CSF-tau levels at diagnosis. Transient high levels of CSF-tau, reaching levels observed in other neurodegenerative disorders, were observed during induction chemotherapy for non-B-ALL, B-NHL and CNS + AML. The clinical implications of both observations will be the subject of further study. Leukemia

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Disease- and treatment-related elevation of the neurodegenerative marker tau in children with hematological malignancies

et al. 2000

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“…This assumption is based on the findings that in acute conditions such as stroke, there is a marked transient increase in CSF T-tau that shows a correlation with computerized tomography measurements of infarct size. 18 Furthermore, the highest increase in CSF T-tau is found in disorders with very intense neuronal degeneration, such as CreutzfeldtJakob disease (CJD), 19 whereas a moderate to marked increase is found in AD with less intense degeneration, 20 and normal levels are found in patients with depression, with limited or no degeneration. 14 CSF P-tau.…”

Section: Tau Proteinmentioning

confidence: 99%

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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Summary:The introduction of acetylcholine esterase (AChE) inhibitors as a symptomatic treatment of Alzheimer's disease (AD) has made patients seek medical advice at an earlier stage of the disease. This has highlighted the importance of diagnostic markers for early AD. However, there is no clinical method to determine which of the patients with mild cognitive impairment (MCI) will progress to AD with dementia, and which have a benign form of MCI without progression. In this paper, the performance of cerebrospinal fluid (CSF) protein biomarkers for AD is reviewed. The diagnostic performance of the three biomarkers, total tau, phospho-tau, and the 42 amino acid form of ␤-amyloid have been evaluated in numerous studies and their ability to identify incipient AD in MCI cases has also been studied. Some candidate AD biomarkers including ubiquitin, neurofilament proteins, growth-associated protein 43 (neuromodulin), and neuronal thread protein (AD7c) show interesting results but have been less extensively studied. It is concluded that CSF biomarkers may have clinical utility in the differentiation between AD and several important differential diagnoses, including normal aging, depression, alcohol dementia, and Parkinson's disease, and also in the identification of Creutzfeldt-Jakob disease in cases with rapidly progressive dementia. Early diagnosis of AD is not only of importance to be able to initiate symptomatic treatment with AChE inhibitors, but will be the basis for initiation of treatment with drugs aimed at slowing down or arresting the degenerative process, such as ␥-secretase inhibitors, if these prove to affect AD pathology and to have a clinical effect.

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“…Using a commercially available ELISA kit, levels of total Tau protein have been determined in CSF from CJD. Results indicate that as a diagnostic marker of CJD, Tau protein is comparable with 14-3-3 protein detection [75,78]. In addition, Tau protein analysis may be useful for diagnosis of other human TSEs.…”

Section: Tau Proteinsmentioning

confidence: 84%

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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Elevated levels of tau-protein in cerebrospinal fluid of patients with Creutzfeldt–Jakob disease

Cited by 305 publications

References 18 publications

Disease- and treatment-related elevation of the neurodegenerative marker tau in children with hematological malignancies

Disease- and treatment-related elevation of the neurodegenerative marker tau in children with hematological malignancies

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

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

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