Effect of Curcumin on aβ-42 Interaction with and Disruption of Lipid Membrane

Effect of Curcumin on Aβ-42 Interaction with and Disruption of Lipid Membrane

Alzheimer’s disease is a progressive, degenerative disorder most common in individuals 65 and older, affecting approximately 48 million individuals as of 2015. With a life expectancy of 3-9 years post-diagnosis and the high cost of caring for these individuals, viable treatments and prevention medications are necessary.

The main pathological hallmark of AD is the presence of extracellular senile plaques made of amyloid beta (Aβ) protein. Two forms of Aβ are found in AD: Aβ-40 the most abundant, Aβ-42 the most toxic. The toxicity of Aβ protein is related to its capability to bind to the cell membrane which leads to the production of pores and cell death. 

The Chi lab is investigating the protection of lipid membranes via the use of curcumin. In this study, the neuroprotective mechanism of curcumin on the highly toxic Aβ-42 protein was investigated by using a combination of technics: Langmuir Blodgett trough, TEM and fluorescence. First, the capability of curcumin to protect the lipid monolayer against different aggregation forms of Aβ-42 was tested. We showed that the insertion of Aβ-42 into the membrane was reduced in presence of curcumin. Secondly, the effect of curcumin on Aβ-42 aggregation was evaluated. Curcumin didn’t stop the aggregation of Aβ-42, but rather modified the morphology of the fibrils which were more granular. Finally, the surface activity of Aβ-42 co-incubated with curcumin was characterized by an increase of the lag phase.

This study facilitated a better understanding of the molecular mechanism of curcumin’s neuroprotective effect, which could contribute to the development of treatments for AD.