11:30 AM - 12:00 PM
[3Ea11] The molecular mechanism of amyloid β aggregation at lipid membrane interface under a non-equilibrium open system
Alzheimer’s disease (AD) is characterized by the aggregation and accumulation of amyloid β (Aβ) on the surface of the brain cells, but the mechanism of is partially unclear. The interstitial fluid supplies and removes Aβ, keeping the brain in a non-equilibrium condition. However, previous studies have examined the equilibrium close space, ignoring the supply and removal of Aβ. Thus, in the present study, we observed the behavior of Aβ aggregation on the lipid membrane under a non-equilibrium open system constructed in our laboratory. In the non-equilibrium open system, the amount of Aβ monomer adsorbed on the membrane was maintained, which promoted Aβ aggregation. We propose the mechanism in which the amount of adsorption and aggregation of Aβ converges the equilibrium steady state under a close system, which it converges to the non-equilibrium steady state under an open system. In conclusion, our study advocates for the importance of experimental verification under non-equilibrium open space because non-equilibrium open space may be involved in the progression of AD.