Amyloid-beta (A beta) plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Clearance of A beta is a promising therapeutic strategy for AD. We have previously demonstrated that peripheral organs play important roles in the clearance of brain-derived A beta. In the present study, we recruited 46 patients with liver cirrhosis and 46 normal controls and found that plasma A beta 40 and A beta 42 levels were significantly higher in the cirrhosis patients than in the normal controls. Notably, cirrhosis patients with hepatitis B virus (HBV) infection had higher plasma A beta 40 and A beta 42 levels than HBV-negative cirrhosis patients. Besides, cirrhosis patients had significantly higher plasma levels of interleukin-1 beta (IL-1 beta) and IL-6. Plasma tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) levels were not significantly different between the groups. Moreover, we found significant correlations of hepatic functions with plasma A beta 40 and A beta 42 levels. Plasma IL-6 levels were also significantly correlated with plasma A beta 40 levels. However, in the linear regression model, we found significant correlation of plasma A beta 40 levels with hepatic functions, but not with plasma IL-6 levels. Our results indicate that the hepatic dysfunctions might result in decreased peripheral A beta clearance by the liver. Protecting hepatic functions might be helpful for the clearance of brain-derived A beta in the blood.