Effect of Increased IL-1β on Expression of HK in Alzheimer's Disease

Alzheimer's disease (AD) is a neurodegenerative disease characterized by decreased glucose metabolism and increased neuroinflammation. Hexokinase (HK) is the key enzyme of glucose metabolism and is associated with mitochondria to exert its function. Recent studies have demonstrated that the dissociation of HK from mitochondria is enough to activate the NOD-like receptor protein 3 (NLRP3) inflammasome and leads to the release of interleukin-1 beta (IL-1 beta). However, the effect of increased IL-1 beta on the expression of HK is still unclear in AD. In this paper, we used positron emission tomography (PET), Western blotting and immunofluorescence to study the glucose metabolism, and the expression and distribution of HK in AD. Furthermore, we used lipopolysaccharide (LPS), nigericin (Nig), CY-09 and lonidamine (LND) to treat N2a and N2a-sw cells to investigate the link between IL-1 beta and HK in AD. The results show decreased expression of HK and the dissociation of HK from mitochondria in AD. Furthermore, a reduction of the expression of IL-1 beta could increase the expression of HK in AD. These results suggest that inhibiting inflammation may help to restore glucose metabolism in AD.

Automated summary

The study found that in AD patients, there is decreased expression of HK and dissociation of HK from mitochondria. Furthermore, reducing the expression of IL-1 beta can increase the expression of HK in AD. These results suggest that inhibiting inflammation may help restore glucose metabolism in AD.