posted on 2021-04-07, 13:36authored byMing-Jang Chiu, Shieh-Yueh Yang, Ta-Fu Chen, Chin-Hsien Lin, Fu-Chi Yang, Wen-Ping Chen, Henrik Zetterberg, Kaj Blennow
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.