The Levels of Tau Isoforms Containing Exon-2 and Exon-10 Segments Increased in the Cerebrospinal Fluids of the Patients with Sporadic Creutzfeldt-Jakob Disease

Chen, Cao; Zhou, Wei; Lv, Yan; Shi, Qi; Wang, Jing; Xiao, Kang; Chen, Lina; Zhang, Bao-Yun; Dong, Xiao-Ping

doi:10.1007/s12035-015-9348-2

Cited by 5 publications

(4 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Total tau level in CSF was quantified using an enzyme‐linked immunosorbent assay (ELISA) kit (INNOTEST hTAU Ag; Immunogenetics, Ghent, Belgium), as described previously [12]. Briefly, 25 μl of the CSF sample was added to each well, and absorbance of each sample was measured at 450 nm on a microplate reader (Thermo) after terminating the reaction by the addition of 2 M H 2 SO 4 .…”

Section: Methodsmentioning

confidence: 99%

Calmodulin level is significantly increased in the cerebrospinal fluid of patients with sporadic Creutzfeldt‐Jakob disease

Cao

Zhou

et al. 2021

Euro J of Neurology

Self Cite

View full text Add to dashboard Cite

Background and purpose Human prion diseases (PrDs) are a group of fatal and transmissible neurodegenerative disorders that are diagnosed definitively in post mortem brains. Calmodulin (CaM) is a ubiquitous calcium‐binding protein. Increased brain CaM level has been reported in prion‐infected rodent models and some scrapie‐infected cells. However, the putative alteration of CaM in cerebrospinal fluid (CSF) of human PrDs is uncertain. Here, we try to figure out the profiles of CSF CaM in sporadic Creutzfeldt‐Jacob disease. Methods Cerebrospinal fluid samples of 40 Chinese patients with probable sporadic Creutzfeldt‐Jacob disease (sCJD) and 40 cases without sCJD (non‐PrDs) were recruited in this study. The presence of CaM in the CSF was assessed by Western blot, while total tau levels were measured using an enzyme‐linked immunosorbent assay kit. In addition, the presence of CaM in another CSF panel consisting of 30 definite sCJD cases and 30 non‐PrD cases was evaluated using CaM‐specific Western blot analysis. Results Cerebrospinal fluid CaM positivity was observed in 28/40 cases of probable sCJD and in 9/40 non‐PrD cases. The CSF tau levels in the probable sCJD cases were markedly higher than those in the non‐PrD cases. Logistic regression established a significant correlation between CSF CaM signal and total CSF tau level. Similar results were observed in the panel of cases with definite sCJD: the rates of CSF CaM positivity in the definite sCJD cases and the non‐PrD cases were 22/30 and 6/30, respectively. Conclusions Although CSF CaM positivity might not be a sCJD‐specific phenomenon, a significantly high rate of CaM‐positive CSF in sCJD cases, especially in those with high CSF tau levels, rendered it a valuable diagnostic biomarker for sCJD.

show abstract

Section: Methodsmentioning

confidence: 99%

Calmodulin level is significantly increased in the cerebrospinal fluid of patients with sporadic Creutzfeldt‐Jakob disease

Cao

Zhou

et al. 2021

Euro J of Neurology

Self Cite

View full text Add to dashboard Cite

show abstract

“…32 Various kinds of abnormal tau pathology have been also described in different types of prion diseases, such as the aberrant phosphorylation of tau, alterations of tau isoforms. [33][34][35][36] Increase of tau in CSF samples is used as diagnostic criteria for sCJD in many countries. However, large amount of NFT in brain is not frequently observed in prion diseases.…”

Section: Increases Of A1-act In Prion Infectionmentioning

confidence: 99%

Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection

Chen

Zhang

et al. 2017

Prion

Self Cite

View full text Add to dashboard Cite

α1-Antichymotrypsin (α1-ACT) belongs to a kind of acute-phase inflammatory protein. Recently, such protein has been proved exist in the amyloid deposits which is the hallmark of Alzheimer's disease, but limitedly reported in prion disease. To estimate the change of α1-ACT during prion infection, the levels of α1-ACT in the brain tissues of scrapie agents 263K-, 139A- and ME7-infected rodents were analyzed, respectively. Results shown that α1-ACT levels were significantly increased in the brain tissues of the three kinds of scrapie-infected rodents, displaying a time-dependent manner during prion infection. Immunohistochemistry assays revealed the increased α1-ACT mainly accumulated in some cerebral regions of rodents infected with prion, such as cortex, thalamus and cerebellum. Immunofluorescent assays illustrated ubiquitously localization of α1-ACT with GFAP positive astrocytes, Iba1-positive microglia and NeuN-positive neurons. Moreover, double-stained immunofluorescent assays and immunohistochemistry assays using series of brain slices demonstrated close morphological colocalization of α1-ACT signals with that of PrP and PrP in the brain slices of 263K-infected hamster. However, co-immunoprecipitation does not identify any detectable molecular interaction between the endogenous α1-ACT and PrP either in the brain homogenates of 263K-infected hamsters or in the lysates of prion-infected cultured cells. Our data here imply that brain α1-ACT is increased abnormally in various scrapie-infected rodent models. Direct molecular interaction between α1-ACT and PrP seems not to be essential for the morphological colocalization of those two proteins in the brain tissues of prion infection.

show abstract

“…A familial type of CJD caused by a mutation of the prion protein gene at codon 180 resulting in a V being changed to isoleucine is found in 40% of all prion diseases, but in Europe, only one case has been reported. 23 The onset age range is 44…”

Section: V180i Mutant Cjdmentioning

confidence: 99%

“…The profiles of tau isoforms in the CSF of CJD patients were used to generate exon‐specific antibodies against the peptides encoded by exon 2, exon 3 and exon 10 of human tau protein, and to evaluate the reactive profiles of tau in CSF samples from patients with probable CJD 44 …”

Section: Laboratory Findings (Eeg Mri Csf)mentioning

confidence: 99%

Human prion disease

Satoh

Nakamura

2021

Clinical & Exp Neuroim

View full text Add to dashboard Cite

Human prion diseases (HPDs) are progressive and fatal neurodegenerative diseases caused by abnormal prion protein (PrP Sc ). They can be sporadic, genetic or acquired.Sporadic HPDs include sporadic Creutzfeldt-Jakob disease (CJD) and sporadic fatal insomnia. Genetic HPDs include genetic CJD, Gerstman-Sträussler-Scheinker disease and fatal familial insomnia. Acquired HPDs include Kuru, variant CJD and iatrogenic CJD. The World Health Organization clinical diagnostic criteria for HPDs include clinical findings, cerebrospinal fluid protein markers and electroencephalography, and the UK and European clinical diagnostic criteria include a combination of clinical findings, 14-3-3 protein in the cerebrospinal fluid, magnetic resonance imaging diffusion-weighted imaging and electroencephalography. Recently, the development and clinical application of real-time quaking-induced conversion has allowed premortem diagnosis of sporadic CJD. The real-time quaking-induced conversion assay allows detection of >1 fg of PrP Sc in diluted CJD brain homogenate, as well as a variety of biological tissues and cerebrospinal fluid. However, the real-time quaking-induced conversion assay does not provide prognostic data and has lower diagnostic accuracy for some rarer, atypical prion diseases. Furthermore, recent advancements in laboratory testing and magnetic resonance imaging diffusion-weighted imaging have shown improved diagnostic accuracy for prion diseases. Clinical trials of prion disease treatments have recently begun in many countries. The therapeutic window consists mainly of the early stage of disease, and few clinical studies have examined the role of biomarkers at this stage. Therefore, biomarkers, imaging and clinical symptoms might be extremely important for the diagnosis of prion diseases. Clinical trials of prion disease treatments have recently begun in many countries. The therapeutic window mainly consists of the early stage of disease, and few clinical studies have examined the role of biomarkers at this stage. Therefore, biomarkers, imaging and clinical symptoms might be extremely important for the diagnosis of prion diseases.

show abstract

The Levels of Tau Isoforms Containing Exon-2 and Exon-10 Segments Increased in the Cerebrospinal Fluids of the Patients with Sporadic Creutzfeldt-Jakob Disease

Cited by 5 publications

References 35 publications

Calmodulin level is significantly increased in the cerebrospinal fluid of patients with sporadic Creutzfeldt‐Jakob disease

Calmodulin level is significantly increased in the cerebrospinal fluid of patients with sporadic Creutzfeldt‐Jakob disease

Remarkable increases of α1-antichymotrypsin in brain tissues of rodents during prion infection

Human prion disease

Contact Info

Product

Resources

About