Chiu, M-J;
              
      
            
                Yang, S-Y;
              
      
            
                Chen, T-F;
              
      
            
                Lin, C-H;
              
      
            
                Yang, F-C;
              
      
            
                Chen, W-P;
              
      
            
                Zetterberg, H;
              
      
            
            
          
      
        
        
        
    
  
(2021)
  Synergistic Association between Plasma Aβ1-42 and p-tau in Alzheimer's Disease but Not in Parkinson's Disease or Frontotemporal Dementia.
ACS Chemical Neuroscience
      
    
    
    
         10.1021/acschemneuro.1c00010.
   (In press).
  
       
    
  
| Preview | Text acschemneuro.1c00010.pdf - Published Version Download (1MB) | Preview | 
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.
| Type: | Article | 
|---|---|
| Title: | Synergistic Association between Plasma Aβ1-42 and p-tau in Alzheimer's Disease but Not in Parkinson's Disease or Frontotemporal Dementia | 
| Location: | United States | 
| Open access status: | An open access version is available from UCL Discovery | 
| DOI: | 10.1021/acschemneuro.1c00010 | 
| Publisher version: | http://dx.doi.org/10.1021/acschemneuro.1c00010 | 
| Language: | English | 
| Additional information: | This article is published under a Creative Commons licence Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) (https://creativecommons.org/licenses/by-nc-nd/4.0/) | 
| Keywords: | Alzheimer’s disease, Parkinson’s disease, Plasma biomarkers, frontotemporal dementia, phosphorylated-tau protein, β-amyloid | 
| UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Neurodegenerative Diseases | 
| URI: | https://discovery.ucl.ac.uk/id/eprint/10126257 | 
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