scholarly journals Follow-Up Investigations of Tau Protein and S-100B Levels in Cerebrospinal Fluid of Patients with Creutzfeldt-Jakob Disease

2005 ◽  
Vol 19 (5-6) ◽  
pp. 376-382 ◽  
Author(s):  
Lukas Cepek ◽  
Petra Steinacker ◽  
Brit Mollenhauer ◽  
Birgitt Wiese ◽  
Barbara Ciesielczyk ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Jakob Disease

Total Tau Protein in Cerebrospinal Fluid and Diffusion-Weighted MRI as an Early Diagnostic Marker for Creutzfeldt-Jakob Disease

2007 ◽  
Vol 24 (3) ◽  
pp. 207-212 ◽  
Author(s):  
Katsuya Satoh ◽  
Susumu Shirabe ◽  
Akira Tsujino ◽  
Hiroto Eguchi ◽  
Masakatsu Motomura ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Diagnostic Marker ◽  
Diffusion Weighted Mri ◽  
Total Tau ◽  
Diffusion Weighted ◽  
Jakob Disease ◽  
And Diffusion ◽  
Early Diagnostic

Elevated Levels of Tau Protein in Cerebrospinal Fluid of Patients With Probable Creutzfeldt-Jakob Disease

2010 ◽  
Vol 340 (4) ◽  
pp. 291-295 ◽  
Author(s):  
Gui-Rong Wang ◽  
Chen Gao ◽  
Qi Shi ◽  
Wei Zhou ◽  
Jian-Ming Chen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Jakob Disease

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

1997 ◽  
Vol 225 (3) ◽  
pp. 210-212 ◽  
Author(s):  
Markus Otto ◽  
Jens Wiltfang ◽  
Hayrettin Tumani ◽  
Inga Zerr ◽  
Maria Lantsch ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Jakob Disease

scholarly journals Drug-induced Creutzfeldt-Jakob disease-like syndrome: early CSF analysis as useful tool for differential diagnosis

2018 ◽  
Vol 11 (1) ◽  
pp. e224314 ◽  
Author(s):  
Federico Paolini Paoletti ◽  
Maria Di Gregorio ◽  
Paolo Calabresi ◽  
Lucilla Parnetti
Keyword(s):  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Tricyclic Antidepressants ◽  
Protein A ◽  
Drug Induced ◽  
Clinical Recovery ◽  
Csf Analysis ◽  
Diagnostic Usefulness ◽  
Jakob Disease ◽  
Rule Out

We report the case of a 78-year-old man who showed a subacute onset of severe cognitive impairment, ataxia, tremor, stimulus sensitive myoclonus and hypophonia. Since a few weeks, he received a treatment with a combination of tricyclic antidepressants for mood disorder. The clinical picture mimicked Creutzfeldt-Jakob disease (CJD), but we could rule out this diagnosis by means of cerebrospinal fluid (CSF) analysis, which showed normal level of tau protein and Aβ1-42, being also negative for CSF 14-3-3 protein. A complete clinical recovery was observed after the discontinuation of antidepressants. So far, some cases of drug-induced CJD-like syndrome have been described. In our experience, early CSF analysis shows high diagnostic usefulness in order to exclude CJD.

Event-related Potentials Improve the Efficiency of Cerebrospinal Fluid Biomarkers for Differential Diagnosis of Alzheimer’s Disease

2018 ◽  
Vol 15 (13) ◽  
pp. 1244-1260 ◽  
Author(s):  
Mirjana Babić Leko ◽  
Magdalena Krbot Skorić ◽  
Nataša Klepac ◽  
Fran Borovečki ◽  
Lea Langer Horvat ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cerebrospinal Fluid ◽  
Differential Diagnosis ◽  
Tau Protein ◽  
Strong Correlation ◽  
Event Related Potentials ◽  
P300 Latency ◽  
Protein Biomarkers ◽  
Related Potentials ◽  
T Tau

Introduction: The pathological process of Alzheimer's disease (AD) in the brain likely begins 20-30 years earlier than the emergence of its first clinical symptoms and symptoms of AD often overlap with the symptoms of other primary causes of dementia. Therefore, it is crucially important to improve early and differential diagnosis of the disease. Event-related potentials (ERP) measured non-invasively by electroencephalography have shown diagnostic potential in AD. Aims: The aim of this study was to compare the efficiency of P300 and N200 potentials and reaction time (RT) with commonly used protein biomarkers measured in the cerebrospinal fluid (CSF), including amyloid β peptide (β1-42), total tau (t-tau), tau protein phosphorylated at threonine 181 (p-tau181), tau protein phosphorylated at serine 199 (p-tau199), tau protein phosphorylated at threonine 231 (p-tau231), and visinin-like protein 1 (VILIP-1) in differential diagnosis of AD in mild cognitive impairment (MCI) and AD patients. Subjects: The study involved 49 AD patients, 28 patients with MCI, 4 healthy control subjects and 16 patients with other primary causes of dementia. Results: ERP (P300RT, N200RT, P300 counting and N200 counting) showed a moderate to strong correlation with protein CSF biomarkers. We confirmed previous observations of moderate to strong correlation between ERP and neuropsychological testing and showed that P300 latency and RT are shortened in AD patients on therapy with acetylcholinesterase inhibitors. Using ERP and RT, a predictive model for determination of AD likelihood in MCI patients was developed, detecting 56.3% of MCI patients with high risk for development of AD in our cohort. MCI patients with pathological levels of Aβ1-42 had prolonged P300 latency, indicating that a combination of ERP and CSF protein biomarkers could improve the differential diagnosis of AD in MCI patients. Additionally, the results suggested the potential of P300 latency in differentiating AD and FTD patients. Conclusion: Our data provide possible solutions for improvement of differential diagnosis of AD, and reveal that the diagnostic efficiency of CSF protein biomarkers t-tau, p-tau181, p-tau199, p-tau231 and VILIP-1 could be improved by adding ERP in clinical practice.

Extremely Elevated Cerebrospinal Fluid Protein and Glucose Level in a Neonate with Hypernatremic Dehydration

2020 ◽  
Author(s):  
Arti Maria ◽  
Tapas Bandyopadhyay
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurodevelopmental Outcome ◽  
Neurological Sequelae ◽  
Glucose Levels ◽  
Csf Analysis ◽  
First Case ◽  
Time Of Admission ◽  
Cerebrospinal Fluid Protein ◽  
Hypernatremic Dehydration

AbstractWe describe the case of a term newborn who presented with hypernatremic dehydration on day 19 of life. The baby was otherwise hemodynamically stable with no evidence of focal or asymmetric neurological signs. The laboratory tests at the time of admission were negative except for hypernatremia and the extremely elevated levels of cerebrospinal fluid (CSF) protein (717 mg/dL) and glucose levels (97 mg/dL). The hypernatremic dehydration was corrected as per the unit protocol over 48 hours. Repeat CSF analysis done after 5 days showed normalization of the protein and glucose levels. Serial follow-up and neuroimaging showed no evidence of neurological sequelae. Unique feature of our case is this is the first case reporting such an extreme elevation of CSF protein and glucose levels that have had no bearing on neurodevelopmental outcome at 1 month and 3 months of follow-up.

Increased levels of total tau protein in the cerebrospinal fluid in Huntington’s disease

2011 ◽  
Vol 17 (9) ◽  
pp. 714-715 ◽  
Author(s):  
Radu Constantinescu ◽  
Megan Romer ◽  
Henrik Zetterberg ◽  
Lars Rosengren ◽  
Karl Kieburtz
Keyword(s):  
Cerebrospinal Fluid ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Tau Protein ◽  
Total Tau

scholarly journals Zebrafish Models to Study New Pathways in Tauopathies

2021 ◽  
Vol 22 (9) ◽  
pp. 4626
Author(s):  
Clément Barbereau ◽  
Nicolas Cubedo ◽  
Tangui Maurice ◽  
Mireille Rossel
Keyword(s):  
Cognitive Deficits ◽  
Tau Protein ◽  
Common Point ◽  
Transgenic Models ◽  
Synaptic Loss ◽  
Wide Range ◽  
Transgenic Lines ◽  
Functional Consequences ◽  
The Common

Tauopathies represent a vast family of neurodegenerative diseases, the most well-known of which is Alzheimer’s disease. The symptoms observed in patients include cognitive deficits and locomotor problems and can lead ultimately to dementia. The common point found in all these pathologies is the accumulation in neural and/or glial cells of abnormal forms of Tau protein, leading to its aggregation and neurofibrillary tangles. Zebrafish transgenic models have been generated with different overexpression strategies of human Tau protein. These transgenic lines have made it possible to highlight Tau interacting factors or factors which may limit the neurotoxicity induced by mutations and hyperphosphorylation of the Tau protein in neurons. Several studies have tested neuroprotective pharmacological approaches. On few-days-old larvae, modulation of various signaling or degradation pathways reversed the deleterious effects of Tau mutations, mainly hTauP301L and hTauA152T. Live imaging and live tracking techniques as well as behavioral follow-up enable the analysis of the wide range of Tau-related phenotypes from synaptic loss to cognitive functional consequences.

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