Chitotriosidase and inflammatory mediator levels in Alzheimer's disease and cerebrovascular dementia

Abstract

Inflammation has been reported to be involved in the pathogenesis of cerebrovascular dementias (CvDs). This study investigated the involvement of Chitotriosidase (ChT), a chinolitic enzyme mainly produced by activated macrophages, in the pathophysiology of Alzheimer's disease (AD) and ischemic CvD. In addition, the levels of interleukin (IL)-16, IL-18, transforming growth factor (TGF)-beta1 and superoxide anion (O2(-)) were determined to evaluate the relationship between ChT levels, these cytokines and oxidative stress in both AD and ischemic CvD patients. The levels of ChT and IL-16, IL-18, and TGF-beta1 mRNA were investigated using quantitative real-time polymerase chain reaction on macrophages of peripheral blood of 40 patients with AD, 40 patients with ischemic CvD and 40 non-demented age-matched subjects. The results show that ChT, IL-16 and O2(-) levels significantly increased in ischemic CvD patients compared with AD patients and were significantly and positively correlated with IL-18 and O2(-). The production of IL-18 was increased in both AD and ischemic CvD patients. TGF-beta1 expression was higher in AD patients and was inversely correlated with the expression of ChT, IL-16 and IL-18, respectively. In non-demented age-matched subjects no significant changes in ChT and IL-16, IL-18, and TGF-beta1 expression were found. Our results indicate that ChT, IL-16, IL-18 and TGF-beta1 are increased in ischemic CvD and AD, confirming that the immune system may play an important role in the development and progression of neurodegenerative disorders. In addition, the present findings suggest that ChT could also play a crucial role in pathological conditions such as CvD in which the inflammatory process is activated.