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- Chiu, Ming-Jang, et al.
(author)
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Synergistic Association between Plasma Aβ1-42 and p-tau in Alzheimer's Disease but Not in Parkinson's Disease or Frontotemporal Dementia.
- 2021
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In: ACS chemical neuroscience. - : American Chemical Society (ACS). - 1948-7193. ; 12:8, s. 1376-1383
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Journal article (peer-reviewed)abstract
- Beta-amyloid (Aβ1-42) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ1-42 in the blood is not elucidated. We investigated the association in individuals with AD (n = 62, including amnesic mild cognitive impairment and dementia), Parkinson's disease (n = 30), frontotemporal dementia (n = 25), and cognitively unimpaired controls (n = 41) using immunomagnetic reduction assays to measure plasma Aβ1-42 and p-tau181 concentrations. Correlation and regression analyses were performed to examine the relation between plasma levels, demographic factors, and clinical severity. Both plasma Aβ1-42 and p-tau concentrations were significantly higher in AD and frontotemporal dementia than in the controls and Parkinson's disease. A significant positive association was found between plasma p-tau and Aβ1-42 in controls (r = 0.579, P < 0.001) and AD (r = 0.699, P < 0.001) but not in frontotemporal dementia or Parkinson's disease. Plasma p-tau was significantly associated with clinical severity in the AD in terms of scores of clinical dementia rating (r = 0.288, P = 0.025) and mini-mental state examination (r = -0.253, P = 0.049). Regression analysis showed that plasma Aβ1-42 levels explain approximately 47.7% of the plasma p-tau levels in the AD after controlling age, gender, and clinical severity. While in non-AD participants, the clinical dementia rating explained about 47.5% of the plasma p-tau levels. The disease-specific association between plasma Aβ1-42 and p-tau levels in AD implies a possible synergic effect in mechanisms involving these two pathological proteins' genesis.
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| 2. |
- Teunissen, Charlotte E, et al.
(author)
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Plasma Amyloid-β (Aβ42) Correlates with Cerebrospinal Fluid Aβ42 in Alzheimer's Disease.
- 2018
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In: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 62:4, s. 1857-1863
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Journal article (peer-reviewed)abstract
- The 42 amino acid form of amyloid-β (Aβ42) plays a key role in the pathogenesis of Alzheimer's disease (AD) and is a core biomarker for the diagnosis of AD. Numerous studies have shown that cerebrospinal fluid (CSF) Aβ42 concentrations are decreased in AD, when measured by enzyme-linked immunosorbent assay (ELISA) and other conventional immunoassays. While most studies report no change in plasma Aβ42, independent studies using the immunomagnetic reduction (IMR) technique report an increase in plasma Aβ42 levels in AD. To confirm the opposite changes of Aβ42 levels in CSF and plasma for AD, we assayed the levels of Aβ42 in plasma of subjects with known CSF Aβ42 levels. In total 43 controls and 63 AD patients were selected at two sites: the VU University Medical Center (n=55) and Sahlgrenska University Hospital (n=51). IMR and ELISA were applied to assay Aβ42 in plasma and CSF, respectively. We found a moderately negative correlation between plasma and CSF Aβ42 levels in AD patients (r=-0.352), and a weakly positive correlation in controls (r=0.186). These findings further corroborate that there are opposite changes of Aβ42 levels in CSF and plasma in AD. The possible causes for the negative correlation are discussed by taken assay technologies, Aβ42 transport from brain to peripheral blood, and sample matrix into account.
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| 3. |
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| 4. |
- Wang, Pei-Ning, et al.
(author)
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Plasma pyroglutamate-modified amyloid beta differentiates amyloid pathology.
- 2020
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In: Alzheimer's & dementia (Amsterdam, Netherlands). - : Wiley. - 2352-8729. ; 12:1
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Journal article (peer-reviewed)abstract
- Pyroglutamate-modified amyloid β (AβpE3) could be a biomarker for Aβ plaque pathology in the brain. An ultra-high-sensitive assay is needed for detecting AβpE3-40.Immunomagnetic reduction was used for quantification of AβpE3-40 in plasma from 46 participants. The concentrations of AβpE3-40 of these subjects were compared with 18F-florbetapir positron emission tomography (PET) images.AβpE3-40 concentration was 44.1 ± 28.2fg/mL in PET- (n = 28) and 91.6 ± 54.6fg/mL in PET+ (n = 18; P < .05). The cutoff value of AβpE3-40 for discriminating PET- from PET+ was 55.5fg/mL, resulting in a sensitivity of 83.3%, a specificity of 71.4%. The concentration of AβpE3-40 showed a moderate correlation (r = 0.437) with PET standardized uptake value ratio.We did not enroll pre-clinical AD subject with normal cognition but Aβ PET+. It would be an important issue to explore the feasibility of using AβpE3-40 for screening pre-clinical subjects.These results reveal the feasibility of detecting Aβ pathology using quantification of a plaque-derived Aβ molecule in plasma.
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