Home > Research > Publications & Outputs > Quantification of plasma phosphorylated tau to ...

Research

Associated organisational unit

Links

Text available via DOI:

Keywords

View graph of relations

Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Published

Standard

Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome. / Tatebe, Harutsugu; Kasai, Takashi; Ohmichi, Takuma et al.
In: Molecular Neurodegeneration, Vol. 12, No. 63, 63, 04.09.2017.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Tatebe, H, Kasai, T, Ohmichi, T, Kishi, Y, Kakeya, T, Waragai, M, Kondo, M, Allsop, D & Tokuda, T 2017, 'Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome', Molecular Neurodegeneration, vol. 12, no. 63, 63. https://doi.org/10.1186/s13024-017-0206-8

APA

Tatebe, H., Kasai, T., Ohmichi, T., Kishi, Y., Kakeya, T., Waragai, M., Kondo, M., Allsop, D., & Tokuda, T. (2017). Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome. Molecular Neurodegeneration, 12(63), Article 63. https://doi.org/10.1186/s13024-017-0206-8

Vancouver

Tatebe H, Kasai T, Ohmichi T, Kishi Y, Kakeya T, Waragai M et al. Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome. Molecular Neurodegeneration. 2017 Sept 4;12(63):63. doi: 10.1186/s13024-017-0206-8

Author

Tatebe, Harutsugu ; Kasai, Takashi ; Ohmichi, Takuma et al. / Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome. In: Molecular Neurodegeneration. 2017 ; Vol. 12, No. 63.

Bibtex

@article{ddb07a400c8c42aea23cbe0a586c21cd,
title = "Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer{\textquoteright}s disease and Down syndrome",
abstract = "Background: There is still a substantial unmet need for less invasive and lower-cost blood-based biomarkers to detect brain Alzheimer{\textquoteright}s disease (AD) pathology. This study is aimed to determine whether quantification of plasma tau phosphorylated at threonine 181 (p-tau181) is informative in the diagnosis of AD. Methods: We have developed a novel ultrasensitive immunoassay to quantify plasma p-tau181, and measured the levels of plasma p-tau181 in three cohorts. Results: In the first cohort composed of 20 AD patients and 15 age-matched controls, the plasma levels of p-tau181 were significantly higher in the AD patients than those in the controls (0.171 ± 0.166 pg/ml in AD versus 0.0405 ± 0.0756 pg/ml in controls, p = 0.0039). The percentage of the subjects whose levels of plasma p-tau181 exceeded the cut-off value (0.0921 pg/ml) was significantly higher in the AD group compared with the control group (60% in AD versus 16.7% in controls, p = 0.0090). In the second cohort composed of 20 patients with Down syndrome (DS) and 22 age-matched controls, the plasma concentrations of p-tau181 were significantly higher in the DS group (0.767 ± 1.26 pg/ml in DS versus 0.0415 ± 0.0710 pg/ml in controls, p = 0.0313). There was a significant correlation between the plasma levels of p-tau181 and age in the DS group (R2 = 0.4451, p = 0.0013). All of the DS individuals showing an extremely high concentration of plasma p-tau181 (> 1.0 pg/ml) were older than the age of 40. In the third cohort composed of 8 AD patients and 3 patients with other neurological diseases, the levels of plasma p-tau181 significantly correlated with those of CSF p-tau181 (R2 = 0.4525, p = 0.023). Conclusions: We report for the first time quantitative data on the plasma levels of p-tau181 in controls and patients with AD and DS, and these data suggest that the plasma p-tau181 is a promising blood biomarker for brain AD pathology. This exploratory pilot study warrants further large-scale and well-controlled studies to validate the usefulness of plasma p-tau181 as an urgently needed surrogate marker for the diagnosis and disease progression of AD. ",
keywords = " Plasma biomarker, Tau phosphorylated at threonine 181 (p-tau181), Simoa, Alzheimer{\textquoteright}s disease, Down's syndrome",
author = "Harutsugu Tatebe and Takashi Kasai and Takuma Ohmichi and Yasuke Kishi and Tomoshi Kakeya and Masaaki Waragai and Masaki Kondo and David Allsop and Takahiko Tokuda",
year = "2017",
month = sep,
day = "4",
doi = "10.1186/s13024-017-0206-8",
language = "English",
volume = "12",
journal = "Molecular Neurodegeneration",
issn = "1750-1326",
publisher = "Springer Nature",
number = "63",

}

RIS

TY - JOUR

T1 - Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer’s disease and Down syndrome

AU - Tatebe, Harutsugu

AU - Kasai, Takashi

AU - Ohmichi, Takuma

AU - Kishi, Yasuke

AU - Kakeya, Tomoshi

AU - Waragai, Masaaki

AU - Kondo, Masaki

AU - Allsop, David

AU - Tokuda, Takahiko

PY - 2017/9/4

Y1 - 2017/9/4

N2 - Background: There is still a substantial unmet need for less invasive and lower-cost blood-based biomarkers to detect brain Alzheimer’s disease (AD) pathology. This study is aimed to determine whether quantification of plasma tau phosphorylated at threonine 181 (p-tau181) is informative in the diagnosis of AD. Methods: We have developed a novel ultrasensitive immunoassay to quantify plasma p-tau181, and measured the levels of plasma p-tau181 in three cohorts. Results: In the first cohort composed of 20 AD patients and 15 age-matched controls, the plasma levels of p-tau181 were significantly higher in the AD patients than those in the controls (0.171 ± 0.166 pg/ml in AD versus 0.0405 ± 0.0756 pg/ml in controls, p = 0.0039). The percentage of the subjects whose levels of plasma p-tau181 exceeded the cut-off value (0.0921 pg/ml) was significantly higher in the AD group compared with the control group (60% in AD versus 16.7% in controls, p = 0.0090). In the second cohort composed of 20 patients with Down syndrome (DS) and 22 age-matched controls, the plasma concentrations of p-tau181 were significantly higher in the DS group (0.767 ± 1.26 pg/ml in DS versus 0.0415 ± 0.0710 pg/ml in controls, p = 0.0313). There was a significant correlation between the plasma levels of p-tau181 and age in the DS group (R2 = 0.4451, p = 0.0013). All of the DS individuals showing an extremely high concentration of plasma p-tau181 (> 1.0 pg/ml) were older than the age of 40. In the third cohort composed of 8 AD patients and 3 patients with other neurological diseases, the levels of plasma p-tau181 significantly correlated with those of CSF p-tau181 (R2 = 0.4525, p = 0.023). Conclusions: We report for the first time quantitative data on the plasma levels of p-tau181 in controls and patients with AD and DS, and these data suggest that the plasma p-tau181 is a promising blood biomarker for brain AD pathology. This exploratory pilot study warrants further large-scale and well-controlled studies to validate the usefulness of plasma p-tau181 as an urgently needed surrogate marker for the diagnosis and disease progression of AD.

AB - Background: There is still a substantial unmet need for less invasive and lower-cost blood-based biomarkers to detect brain Alzheimer’s disease (AD) pathology. This study is aimed to determine whether quantification of plasma tau phosphorylated at threonine 181 (p-tau181) is informative in the diagnosis of AD. Methods: We have developed a novel ultrasensitive immunoassay to quantify plasma p-tau181, and measured the levels of plasma p-tau181 in three cohorts. Results: In the first cohort composed of 20 AD patients and 15 age-matched controls, the plasma levels of p-tau181 were significantly higher in the AD patients than those in the controls (0.171 ± 0.166 pg/ml in AD versus 0.0405 ± 0.0756 pg/ml in controls, p = 0.0039). The percentage of the subjects whose levels of plasma p-tau181 exceeded the cut-off value (0.0921 pg/ml) was significantly higher in the AD group compared with the control group (60% in AD versus 16.7% in controls, p = 0.0090). In the second cohort composed of 20 patients with Down syndrome (DS) and 22 age-matched controls, the plasma concentrations of p-tau181 were significantly higher in the DS group (0.767 ± 1.26 pg/ml in DS versus 0.0415 ± 0.0710 pg/ml in controls, p = 0.0313). There was a significant correlation between the plasma levels of p-tau181 and age in the DS group (R2 = 0.4451, p = 0.0013). All of the DS individuals showing an extremely high concentration of plasma p-tau181 (> 1.0 pg/ml) were older than the age of 40. In the third cohort composed of 8 AD patients and 3 patients with other neurological diseases, the levels of plasma p-tau181 significantly correlated with those of CSF p-tau181 (R2 = 0.4525, p = 0.023). Conclusions: We report for the first time quantitative data on the plasma levels of p-tau181 in controls and patients with AD and DS, and these data suggest that the plasma p-tau181 is a promising blood biomarker for brain AD pathology. This exploratory pilot study warrants further large-scale and well-controlled studies to validate the usefulness of plasma p-tau181 as an urgently needed surrogate marker for the diagnosis and disease progression of AD.

KW - Plasma biomarker

KW - Tau phosphorylated at threonine 181 (p-tau181)

KW - Simoa

KW - Alzheimer’s disease

KW - Down's syndrome

U2 - 10.1186/s13024-017-0206-8

DO - 10.1186/s13024-017-0206-8

M3 - Journal article

VL - 12

JO - Molecular Neurodegeneration

JF - Molecular Neurodegeneration

SN - 1750-1326

IS - 63

M1 - 63

ER -